Long Noncoding RNA FGD5-AS1 Acts as a Competing Endogenous RNA on microRNA-383 to Enhance the Malignant Characteristics of Esophageal Squamous Cell Carcinoma by Increasing SP1 Expression

Jia Gao,1,* Ziteng Zhang,2,* Hong Su,1 Ling Zong,2 Yan Li1 1Department of Thoracic Surgery, Heze Municipal Hospital, Heze, Shandong 274031, People’s Republic of China; 2Department of Thoracic Surgery, Affiliated Hospital of Jining Medical University, Shandong 272000, People’s Republic of China*These authors contributed equally to this workCorrespondence: Yan LiDepartment of Thoracic Surgery, Heze Municipal Hospital, No. 2888 Caozhou West Road, Heze, Shandong 274031, People’s Republic of ChinaEmail yanli_heze163.comPurpose: Previous studies have identified the important roles of a long noncoding RNA called FGD5 antisense RNA 1 (FGD5-AS1) in several types of human cancer. Nonetheless, to our knowledge, the expression and functions of FGD5-AS1 in esophageal squamous cell carcinoma (ESCC) have not been clarified. In this study, we aimed to determine the expression status of long noncoding RNA FGD5-AS1 in ESCC, determine its participation in ESCC progression, and uncover the underlying mechanisms.Methods: ESCC tissue samples and paired normal adjacent tissues were collected to quantify FGD5-AS1 expression by reverse-transcription quantitative PCR. The effects of FGD5-AS1 on ESCC cell proliferation, apoptosis, migration, and invasion in vitro as well as tumor growth in vivo were studied using a Cell Counting Kit-8 assay, flow cytometry, Transwell migration and invasion assays, and an in vivo tumor xenograft experiment.Results: FGD5-AS1 was found to be aberrantly upregulated in both ESCC tumors and cell lines compared to the control groups. Increased FGD5-AS1 expression manifested a close association with tumor size, TNM stage, and lymph node metastasis in patients with ESCC. Overall survival of patients with ESCC was shorter in the FGD5-AS1 high-expression group than in the FGD5-AS1 low-expression group. An FGD5-AS1 knockdown markedly attenuated ESCC cell proliferation, migration, and invasion and promoted apoptosis in vitro as well as slowed tumor growth in vivo. Mechanism investigation revealed that FGD5-AS1 can increase SP1 expression by sponging microRNA-383 (miR-383), thus functioning as a competing endogenous RNA. An miR-383 knockdown and recovery of SP1 expression attenuated the inhibition of the malignant characteristics of ESCC cells by the FGD5-AS1 knockdown.Conclusion: Thus, FGD5-AS1 enhances the aggressive phenotype of ESCC cells in vitro and in vivo via the miR-383–SP1 axis, which may represent a novel target for ESCC therapy.Keywords: esophageal squamous cell carcinoma, FGD5 antisense RNA 1, microRNA-383 Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Gao J [verfasserIn] Zhang Z [verfasserIn] Su H [verfasserIn] Zong L [verfasserIn] Li Y [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2020

Schlagwörter:	esophageal squamous cell carcinoma fgd5 antisense rna 1 microrna-383

Übergeordnetes Werk:	In: Cancer Management and Research - Dove Medical Press, 2009, (2020), Seite 2265-2278
Übergeordnetes Werk:	year:2020 ; pages:2265-2278

Links:	Link aufrufen Link aufrufen Journal toc

Katalog-ID:	DOAJ017286549

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520			\|a Jia Gao,1,* Ziteng Zhang,2,* Hong Su,1 Ling Zong,2 Yan Li1 1Department of Thoracic Surgery, Heze Municipal Hospital, Heze, Shandong 274031, People’s Republic of China; 2Department of Thoracic Surgery, Affiliated Hospital of Jining Medical University, Shandong 272000, People’s Republic of China*These authors contributed equally to this workCorrespondence: Yan LiDepartment of Thoracic Surgery, Heze Municipal Hospital, No. 2888 Caozhou West Road, Heze, Shandong 274031, People’s Republic of ChinaEmail yanli_heze163.comPurpose: Previous studies have identified the important roles of a long noncoding RNA called FGD5 antisense RNA 1 (FGD5-AS1) in several types of human cancer. Nonetheless, to our knowledge, the expression and functions of FGD5-AS1 in esophageal squamous cell carcinoma (ESCC) have not been clarified. In this study, we aimed to determine the expression status of long noncoding RNA FGD5-AS1 in ESCC, determine its participation in ESCC progression, and uncover the underlying mechanisms.Methods: ESCC tissue samples and paired normal adjacent tissues were collected to quantify FGD5-AS1 expression by reverse-transcription quantitative PCR. The effects of FGD5-AS1 on ESCC cell proliferation, apoptosis, migration, and invasion in vitro as well as tumor growth in vivo were studied using a Cell Counting Kit-8 assay, flow cytometry, Transwell migration and invasion assays, and an in vivo tumor xenograft experiment.Results: FGD5-AS1 was found to be aberrantly upregulated in both ESCC tumors and cell lines compared to the control groups. Increased FGD5-AS1 expression manifested a close association with tumor size, TNM stage, and lymph node metastasis in patients with ESCC. Overall survival of patients with ESCC was shorter in the FGD5-AS1 high-expression group than in the FGD5-AS1 low-expression group. An FGD5-AS1 knockdown markedly attenuated ESCC cell proliferation, migration, and invasion and promoted apoptosis in vitro as well as slowed tumor growth in vivo. Mechanism investigation revealed that FGD5-AS1 can increase SP1 expression by sponging microRNA-383 (miR-383), thus functioning as a competing endogenous RNA. An miR-383 knockdown and recovery of SP1 expression attenuated the inhibition of the malignant characteristics of ESCC cells by the FGD5-AS1 knockdown.Conclusion: Thus, FGD5-AS1 enhances the aggressive phenotype of ESCC cells in vitro and in vivo via the miR-383–SP1 axis, which may represent a novel target for ESCC therapy.Keywords: esophageal squamous cell carcinoma, FGD5 antisense RNA 1, microRNA-383
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allfields	(DE-627)DOAJ017286549 (DE-599)DOAJ9430d66b84dc4231986cd4fa1a048f1a DE-627 ger DE-627 rakwb eng RC254-282 Gao J verfasserin aut Long Noncoding RNA FGD5-AS1 Acts as a Competing Endogenous RNA on microRNA-383 to Enhance the Malignant Characteristics of Esophageal Squamous Cell Carcinoma by Increasing SP1 Expression 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Jia Gao,1,* Ziteng Zhang,2,* Hong Su,1 Ling Zong,2 Yan Li1 1Department of Thoracic Surgery, Heze Municipal Hospital, Heze, Shandong 274031, People’s Republic of China; 2Department of Thoracic Surgery, Affiliated Hospital of Jining Medical University, Shandong 272000, People’s Republic of China*These authors contributed equally to this workCorrespondence: Yan LiDepartment of Thoracic Surgery, Heze Municipal Hospital, No. 2888 Caozhou West Road, Heze, Shandong 274031, People’s Republic of ChinaEmail yanli_heze163.comPurpose: Previous studies have identified the important roles of a long noncoding RNA called FGD5 antisense RNA 1 (FGD5-AS1) in several types of human cancer. Nonetheless, to our knowledge, the expression and functions of FGD5-AS1 in esophageal squamous cell carcinoma (ESCC) have not been clarified. In this study, we aimed to determine the expression status of long noncoding RNA FGD5-AS1 in ESCC, determine its participation in ESCC progression, and uncover the underlying mechanisms.Methods: ESCC tissue samples and paired normal adjacent tissues were collected to quantify FGD5-AS1 expression by reverse-transcription quantitative PCR. The effects of FGD5-AS1 on ESCC cell proliferation, apoptosis, migration, and invasion in vitro as well as tumor growth in vivo were studied using a Cell Counting Kit-8 assay, flow cytometry, Transwell migration and invasion assays, and an in vivo tumor xenograft experiment.Results: FGD5-AS1 was found to be aberrantly upregulated in both ESCC tumors and cell lines compared to the control groups. Increased FGD5-AS1 expression manifested a close association with tumor size, TNM stage, and lymph node metastasis in patients with ESCC. Overall survival of patients with ESCC was shorter in the FGD5-AS1 high-expression group than in the FGD5-AS1 low-expression group. An FGD5-AS1 knockdown markedly attenuated ESCC cell proliferation, migration, and invasion and promoted apoptosis in vitro as well as slowed tumor growth in vivo. Mechanism investigation revealed that FGD5-AS1 can increase SP1 expression by sponging microRNA-383 (miR-383), thus functioning as a competing endogenous RNA. An miR-383 knockdown and recovery of SP1 expression attenuated the inhibition of the malignant characteristics of ESCC cells by the FGD5-AS1 knockdown.Conclusion: Thus, FGD5-AS1 enhances the aggressive phenotype of ESCC cells in vitro and in vivo via the miR-383–SP1 axis, which may represent a novel target for ESCC therapy.Keywords: esophageal squamous cell carcinoma, FGD5 antisense RNA 1, microRNA-383 esophageal squamous cell carcinoma fgd5 antisense rna 1 microrna-383 Neoplasms. Tumors. Oncology. Including cancer and carcinogens Zhang Z verfasserin aut Su H verfasserin aut Zong L verfasserin aut Li Y verfasserin aut In Cancer Management and Research Dove Medical Press, 2009 (2020), Seite 2265-2278 (DE-627)606030840 (DE-600)2508013-1 11791322 nnns year:2020 pages:2265-2278 https://doaj.org/article/9430d66b84dc4231986cd4fa1a048f1a kostenfrei https://www.dovepress.com/long-noncoding-rna-fgd5-as1-acts-as-a-competing-endogenous-rna-on-micr-peer-reviewed-article-CMAR kostenfrei https://doaj.org/toc/1179-1322 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 2020 2265-2278
spelling	(DE-627)DOAJ017286549 (DE-599)DOAJ9430d66b84dc4231986cd4fa1a048f1a DE-627 ger DE-627 rakwb eng RC254-282 Gao J verfasserin aut Long Noncoding RNA FGD5-AS1 Acts as a Competing Endogenous RNA on microRNA-383 to Enhance the Malignant Characteristics of Esophageal Squamous Cell Carcinoma by Increasing SP1 Expression 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Jia Gao,1,* Ziteng Zhang,2,* Hong Su,1 Ling Zong,2 Yan Li1 1Department of Thoracic Surgery, Heze Municipal Hospital, Heze, Shandong 274031, People’s Republic of China; 2Department of Thoracic Surgery, Affiliated Hospital of Jining Medical University, Shandong 272000, People’s Republic of China*These authors contributed equally to this workCorrespondence: Yan LiDepartment of Thoracic Surgery, Heze Municipal Hospital, No. 2888 Caozhou West Road, Heze, Shandong 274031, People’s Republic of ChinaEmail yanli_heze163.comPurpose: Previous studies have identified the important roles of a long noncoding RNA called FGD5 antisense RNA 1 (FGD5-AS1) in several types of human cancer. Nonetheless, to our knowledge, the expression and functions of FGD5-AS1 in esophageal squamous cell carcinoma (ESCC) have not been clarified. In this study, we aimed to determine the expression status of long noncoding RNA FGD5-AS1 in ESCC, determine its participation in ESCC progression, and uncover the underlying mechanisms.Methods: ESCC tissue samples and paired normal adjacent tissues were collected to quantify FGD5-AS1 expression by reverse-transcription quantitative PCR. The effects of FGD5-AS1 on ESCC cell proliferation, apoptosis, migration, and invasion in vitro as well as tumor growth in vivo were studied using a Cell Counting Kit-8 assay, flow cytometry, Transwell migration and invasion assays, and an in vivo tumor xenograft experiment.Results: FGD5-AS1 was found to be aberrantly upregulated in both ESCC tumors and cell lines compared to the control groups. Increased FGD5-AS1 expression manifested a close association with tumor size, TNM stage, and lymph node metastasis in patients with ESCC. Overall survival of patients with ESCC was shorter in the FGD5-AS1 high-expression group than in the FGD5-AS1 low-expression group. An FGD5-AS1 knockdown markedly attenuated ESCC cell proliferation, migration, and invasion and promoted apoptosis in vitro as well as slowed tumor growth in vivo. Mechanism investigation revealed that FGD5-AS1 can increase SP1 expression by sponging microRNA-383 (miR-383), thus functioning as a competing endogenous RNA. An miR-383 knockdown and recovery of SP1 expression attenuated the inhibition of the malignant characteristics of ESCC cells by the FGD5-AS1 knockdown.Conclusion: Thus, FGD5-AS1 enhances the aggressive phenotype of ESCC cells in vitro and in vivo via the miR-383–SP1 axis, which may represent a novel target for ESCC therapy.Keywords: esophageal squamous cell carcinoma, FGD5 antisense RNA 1, microRNA-383 esophageal squamous cell carcinoma fgd5 antisense rna 1 microrna-383 Neoplasms. Tumors. Oncology. Including cancer and carcinogens Zhang Z verfasserin aut Su H verfasserin aut Zong L verfasserin aut Li Y verfasserin aut In Cancer Management and Research Dove Medical Press, 2009 (2020), Seite 2265-2278 (DE-627)606030840 (DE-600)2508013-1 11791322 nnns year:2020 pages:2265-2278 https://doaj.org/article/9430d66b84dc4231986cd4fa1a048f1a kostenfrei https://www.dovepress.com/long-noncoding-rna-fgd5-as1-acts-as-a-competing-endogenous-rna-on-micr-peer-reviewed-article-CMAR kostenfrei https://doaj.org/toc/1179-1322 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 2020 2265-2278
allfields_unstemmed	(DE-627)DOAJ017286549 (DE-599)DOAJ9430d66b84dc4231986cd4fa1a048f1a DE-627 ger DE-627 rakwb eng RC254-282 Gao J verfasserin aut Long Noncoding RNA FGD5-AS1 Acts as a Competing Endogenous RNA on microRNA-383 to Enhance the Malignant Characteristics of Esophageal Squamous Cell Carcinoma by Increasing SP1 Expression 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Jia Gao,1,* Ziteng Zhang,2,* Hong Su,1 Ling Zong,2 Yan Li1 1Department of Thoracic Surgery, Heze Municipal Hospital, Heze, Shandong 274031, People’s Republic of China; 2Department of Thoracic Surgery, Affiliated Hospital of Jining Medical University, Shandong 272000, People’s Republic of China*These authors contributed equally to this workCorrespondence: Yan LiDepartment of Thoracic Surgery, Heze Municipal Hospital, No. 2888 Caozhou West Road, Heze, Shandong 274031, People’s Republic of ChinaEmail yanli_heze163.comPurpose: Previous studies have identified the important roles of a long noncoding RNA called FGD5 antisense RNA 1 (FGD5-AS1) in several types of human cancer. Nonetheless, to our knowledge, the expression and functions of FGD5-AS1 in esophageal squamous cell carcinoma (ESCC) have not been clarified. In this study, we aimed to determine the expression status of long noncoding RNA FGD5-AS1 in ESCC, determine its participation in ESCC progression, and uncover the underlying mechanisms.Methods: ESCC tissue samples and paired normal adjacent tissues were collected to quantify FGD5-AS1 expression by reverse-transcription quantitative PCR. The effects of FGD5-AS1 on ESCC cell proliferation, apoptosis, migration, and invasion in vitro as well as tumor growth in vivo were studied using a Cell Counting Kit-8 assay, flow cytometry, Transwell migration and invasion assays, and an in vivo tumor xenograft experiment.Results: FGD5-AS1 was found to be aberrantly upregulated in both ESCC tumors and cell lines compared to the control groups. Increased FGD5-AS1 expression manifested a close association with tumor size, TNM stage, and lymph node metastasis in patients with ESCC. Overall survival of patients with ESCC was shorter in the FGD5-AS1 high-expression group than in the FGD5-AS1 low-expression group. An FGD5-AS1 knockdown markedly attenuated ESCC cell proliferation, migration, and invasion and promoted apoptosis in vitro as well as slowed tumor growth in vivo. Mechanism investigation revealed that FGD5-AS1 can increase SP1 expression by sponging microRNA-383 (miR-383), thus functioning as a competing endogenous RNA. An miR-383 knockdown and recovery of SP1 expression attenuated the inhibition of the malignant characteristics of ESCC cells by the FGD5-AS1 knockdown.Conclusion: Thus, FGD5-AS1 enhances the aggressive phenotype of ESCC cells in vitro and in vivo via the miR-383–SP1 axis, which may represent a novel target for ESCC therapy.Keywords: esophageal squamous cell carcinoma, FGD5 antisense RNA 1, microRNA-383 esophageal squamous cell carcinoma fgd5 antisense rna 1 microrna-383 Neoplasms. Tumors. Oncology. Including cancer and carcinogens Zhang Z verfasserin aut Su H verfasserin aut Zong L verfasserin aut Li Y verfasserin aut In Cancer Management and Research Dove Medical Press, 2009 (2020), Seite 2265-2278 (DE-627)606030840 (DE-600)2508013-1 11791322 nnns year:2020 pages:2265-2278 https://doaj.org/article/9430d66b84dc4231986cd4fa1a048f1a kostenfrei https://www.dovepress.com/long-noncoding-rna-fgd5-as1-acts-as-a-competing-endogenous-rna-on-micr-peer-reviewed-article-CMAR kostenfrei https://doaj.org/toc/1179-1322 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 2020 2265-2278
allfieldsGer	(DE-627)DOAJ017286549 (DE-599)DOAJ9430d66b84dc4231986cd4fa1a048f1a DE-627 ger DE-627 rakwb eng RC254-282 Gao J verfasserin aut Long Noncoding RNA FGD5-AS1 Acts as a Competing Endogenous RNA on microRNA-383 to Enhance the Malignant Characteristics of Esophageal Squamous Cell Carcinoma by Increasing SP1 Expression 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Jia Gao,1,* Ziteng Zhang,2,* Hong Su,1 Ling Zong,2 Yan Li1 1Department of Thoracic Surgery, Heze Municipal Hospital, Heze, Shandong 274031, People’s Republic of China; 2Department of Thoracic Surgery, Affiliated Hospital of Jining Medical University, Shandong 272000, People’s Republic of China*These authors contributed equally to this workCorrespondence: Yan LiDepartment of Thoracic Surgery, Heze Municipal Hospital, No. 2888 Caozhou West Road, Heze, Shandong 274031, People’s Republic of ChinaEmail yanli_heze163.comPurpose: Previous studies have identified the important roles of a long noncoding RNA called FGD5 antisense RNA 1 (FGD5-AS1) in several types of human cancer. Nonetheless, to our knowledge, the expression and functions of FGD5-AS1 in esophageal squamous cell carcinoma (ESCC) have not been clarified. In this study, we aimed to determine the expression status of long noncoding RNA FGD5-AS1 in ESCC, determine its participation in ESCC progression, and uncover the underlying mechanisms.Methods: ESCC tissue samples and paired normal adjacent tissues were collected to quantify FGD5-AS1 expression by reverse-transcription quantitative PCR. The effects of FGD5-AS1 on ESCC cell proliferation, apoptosis, migration, and invasion in vitro as well as tumor growth in vivo were studied using a Cell Counting Kit-8 assay, flow cytometry, Transwell migration and invasion assays, and an in vivo tumor xenograft experiment.Results: FGD5-AS1 was found to be aberrantly upregulated in both ESCC tumors and cell lines compared to the control groups. Increased FGD5-AS1 expression manifested a close association with tumor size, TNM stage, and lymph node metastasis in patients with ESCC. Overall survival of patients with ESCC was shorter in the FGD5-AS1 high-expression group than in the FGD5-AS1 low-expression group. An FGD5-AS1 knockdown markedly attenuated ESCC cell proliferation, migration, and invasion and promoted apoptosis in vitro as well as slowed tumor growth in vivo. Mechanism investigation revealed that FGD5-AS1 can increase SP1 expression by sponging microRNA-383 (miR-383), thus functioning as a competing endogenous RNA. An miR-383 knockdown and recovery of SP1 expression attenuated the inhibition of the malignant characteristics of ESCC cells by the FGD5-AS1 knockdown.Conclusion: Thus, FGD5-AS1 enhances the aggressive phenotype of ESCC cells in vitro and in vivo via the miR-383–SP1 axis, which may represent a novel target for ESCC therapy.Keywords: esophageal squamous cell carcinoma, FGD5 antisense RNA 1, microRNA-383 esophageal squamous cell carcinoma fgd5 antisense rna 1 microrna-383 Neoplasms. Tumors. Oncology. Including cancer and carcinogens Zhang Z verfasserin aut Su H verfasserin aut Zong L verfasserin aut Li Y verfasserin aut In Cancer Management and Research Dove Medical Press, 2009 (2020), Seite 2265-2278 (DE-627)606030840 (DE-600)2508013-1 11791322 nnns year:2020 pages:2265-2278 https://doaj.org/article/9430d66b84dc4231986cd4fa1a048f1a kostenfrei https://www.dovepress.com/long-noncoding-rna-fgd5-as1-acts-as-a-competing-endogenous-rna-on-micr-peer-reviewed-article-CMAR kostenfrei https://doaj.org/toc/1179-1322 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 2020 2265-2278
allfieldsSound	(DE-627)DOAJ017286549 (DE-599)DOAJ9430d66b84dc4231986cd4fa1a048f1a DE-627 ger DE-627 rakwb eng RC254-282 Gao J verfasserin aut Long Noncoding RNA FGD5-AS1 Acts as a Competing Endogenous RNA on microRNA-383 to Enhance the Malignant Characteristics of Esophageal Squamous Cell Carcinoma by Increasing SP1 Expression 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Jia Gao,1,* Ziteng Zhang,2,* Hong Su,1 Ling Zong,2 Yan Li1 1Department of Thoracic Surgery, Heze Municipal Hospital, Heze, Shandong 274031, People’s Republic of China; 2Department of Thoracic Surgery, Affiliated Hospital of Jining Medical University, Shandong 272000, People’s Republic of China*These authors contributed equally to this workCorrespondence: Yan LiDepartment of Thoracic Surgery, Heze Municipal Hospital, No. 2888 Caozhou West Road, Heze, Shandong 274031, People’s Republic of ChinaEmail yanli_heze163.comPurpose: Previous studies have identified the important roles of a long noncoding RNA called FGD5 antisense RNA 1 (FGD5-AS1) in several types of human cancer. Nonetheless, to our knowledge, the expression and functions of FGD5-AS1 in esophageal squamous cell carcinoma (ESCC) have not been clarified. In this study, we aimed to determine the expression status of long noncoding RNA FGD5-AS1 in ESCC, determine its participation in ESCC progression, and uncover the underlying mechanisms.Methods: ESCC tissue samples and paired normal adjacent tissues were collected to quantify FGD5-AS1 expression by reverse-transcription quantitative PCR. The effects of FGD5-AS1 on ESCC cell proliferation, apoptosis, migration, and invasion in vitro as well as tumor growth in vivo were studied using a Cell Counting Kit-8 assay, flow cytometry, Transwell migration and invasion assays, and an in vivo tumor xenograft experiment.Results: FGD5-AS1 was found to be aberrantly upregulated in both ESCC tumors and cell lines compared to the control groups. Increased FGD5-AS1 expression manifested a close association with tumor size, TNM stage, and lymph node metastasis in patients with ESCC. Overall survival of patients with ESCC was shorter in the FGD5-AS1 high-expression group than in the FGD5-AS1 low-expression group. An FGD5-AS1 knockdown markedly attenuated ESCC cell proliferation, migration, and invasion and promoted apoptosis in vitro as well as slowed tumor growth in vivo. Mechanism investigation revealed that FGD5-AS1 can increase SP1 expression by sponging microRNA-383 (miR-383), thus functioning as a competing endogenous RNA. An miR-383 knockdown and recovery of SP1 expression attenuated the inhibition of the malignant characteristics of ESCC cells by the FGD5-AS1 knockdown.Conclusion: Thus, FGD5-AS1 enhances the aggressive phenotype of ESCC cells in vitro and in vivo via the miR-383–SP1 axis, which may represent a novel target for ESCC therapy.Keywords: esophageal squamous cell carcinoma, FGD5 antisense RNA 1, microRNA-383 esophageal squamous cell carcinoma fgd5 antisense rna 1 microrna-383 Neoplasms. Tumors. Oncology. Including cancer and carcinogens Zhang Z verfasserin aut Su H verfasserin aut Zong L verfasserin aut Li Y verfasserin aut In Cancer Management and Research Dove Medical Press, 2009 (2020), Seite 2265-2278 (DE-627)606030840 (DE-600)2508013-1 11791322 nnns year:2020 pages:2265-2278 https://doaj.org/article/9430d66b84dc4231986cd4fa1a048f1a kostenfrei https://www.dovepress.com/long-noncoding-rna-fgd5-as1-acts-as-a-competing-endogenous-rna-on-micr-peer-reviewed-article-CMAR kostenfrei https://doaj.org/toc/1179-1322 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 2020 2265-2278
language	English
source	In Cancer Management and Research (2020), Seite 2265-2278 year:2020 pages:2265-2278
sourceStr	In Cancer Management and Research (2020), Seite 2265-2278 year:2020 pages:2265-2278
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	esophageal squamous cell carcinoma fgd5 antisense rna 1 microrna-383 Neoplasms. Tumors. Oncology. Including cancer and carcinogens
isfreeaccess_bool	true
container_title	Cancer Management and Research
authorswithroles_txt_mv	Gao J @@aut@@ Zhang Z @@aut@@ Su H @@aut@@ Zong L @@aut@@ Li Y @@aut@@
publishDateDaySort_date	2020-01-01T00:00:00Z
hierarchy_top_id	606030840
id	DOAJ017286549
language_de	englisch
fullrecord	<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">DOAJ017286549</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230502212954.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230226s2020 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ017286549</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJ9430d66b84dc4231986cd4fa1a048f1a</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">RC254-282</subfield></datafield><datafield tag="100" ind1="0" ind2=" "><subfield code="a">Gao J</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Long Noncoding RNA FGD5-AS1 Acts as a Competing Endogenous RNA on microRNA-383 to Enhance the Malignant Characteristics of Esophageal Squamous Cell Carcinoma by Increasing SP1 Expression</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2020</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Jia Gao,1,* Ziteng Zhang,2,* Hong Su,1 Ling Zong,2 Yan Li1 1Department of Thoracic Surgery, Heze Municipal Hospital, Heze, Shandong 274031, People&rsquo;s Republic of China; 2Department of Thoracic Surgery, Affiliated Hospital of Jining Medical University, Shandong 272000, People&rsquo;s Republic of China*These authors contributed equally to this workCorrespondence: Yan LiDepartment of Thoracic Surgery, Heze Municipal Hospital, No. 2888 Caozhou West Road, Heze, Shandong 274031, People&rsquo;s Republic of ChinaEmail yanli_heze163.comPurpose: Previous studies have identified the important roles of a long noncoding RNA called FGD5 antisense RNA 1 (FGD5-AS1) in several types of human cancer. Nonetheless, to our knowledge, the expression and functions of FGD5-AS1 in esophageal squamous cell carcinoma (ESCC) have not been clarified. In this study, we aimed to determine the expression status of long noncoding RNA FGD5-AS1 in ESCC, determine its participation in ESCC progression, and uncover the underlying mechanisms.Methods: ESCC tissue samples and paired normal adjacent tissues were collected to quantify FGD5-AS1 expression by reverse-transcription quantitative PCR. The effects of FGD5-AS1 on ESCC cell proliferation, apoptosis, migration, and invasion in vitro as well as tumor growth in vivo were studied using a Cell Counting Kit-8 assay, flow cytometry, Transwell migration and invasion assays, and an in vivo tumor xenograft experiment.Results: FGD5-AS1 was found to be aberrantly upregulated in both ESCC tumors and cell lines compared to the control groups. Increased FGD5-AS1 expression manifested a close association with tumor size, TNM stage, and lymph node metastasis in patients with ESCC. Overall survival of patients with ESCC was shorter in the FGD5-AS1 high-expression group than in the FGD5-AS1 low-expression group. An FGD5-AS1 knockdown markedly attenuated ESCC cell proliferation, migration, and invasion and promoted apoptosis in vitro as well as slowed tumor growth in vivo. Mechanism investigation revealed that FGD5-AS1 can increase SP1 expression by sponging microRNA-383 (miR-383), thus functioning as a competing endogenous RNA. An miR-383 knockdown and recovery of SP1 expression attenuated the inhibition of the malignant characteristics of ESCC cells by the FGD5-AS1 knockdown.Conclusion: Thus, FGD5-AS1 enhances the aggressive phenotype of ESCC cells in vitro and in vivo via the miR-383&ndash;SP1 axis, which may represent a novel target for ESCC therapy.Keywords: esophageal squamous cell carcinoma, FGD5 antisense RNA 1, microRNA-383</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">esophageal squamous cell carcinoma</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">fgd5 antisense rna 1</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">microrna-383</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Neoplasms. Tumors. Oncology. 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callnumber-first	R - Medicine
author	Gao J
spellingShingle	Gao J misc RC254-282 misc esophageal squamous cell carcinoma misc fgd5 antisense rna 1 misc microrna-383 misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens Long Noncoding RNA FGD5-AS1 Acts as a Competing Endogenous RNA on microRNA-383 to Enhance the Malignant Characteristics of Esophageal Squamous Cell Carcinoma by Increasing SP1 Expression
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topic_title	RC254-282 Long Noncoding RNA FGD5-AS1 Acts as a Competing Endogenous RNA on microRNA-383 to Enhance the Malignant Characteristics of Esophageal Squamous Cell Carcinoma by Increasing SP1 Expression esophageal squamous cell carcinoma fgd5 antisense rna 1 microrna-383
topic	misc RC254-282 misc esophageal squamous cell carcinoma misc fgd5 antisense rna 1 misc microrna-383 misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens
topic_unstemmed	misc RC254-282 misc esophageal squamous cell carcinoma misc fgd5 antisense rna 1 misc microrna-383 misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens
topic_browse	misc RC254-282 misc esophageal squamous cell carcinoma misc fgd5 antisense rna 1 misc microrna-383 misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens
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title	Long Noncoding RNA FGD5-AS1 Acts as a Competing Endogenous RNA on microRNA-383 to Enhance the Malignant Characteristics of Esophageal Squamous Cell Carcinoma by Increasing SP1 Expression
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title_full	Long Noncoding RNA FGD5-AS1 Acts as a Competing Endogenous RNA on microRNA-383 to Enhance the Malignant Characteristics of Esophageal Squamous Cell Carcinoma by Increasing SP1 Expression
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title_sort	long noncoding rna fgd5-as1 acts as a competing endogenous rna on microrna-383 to enhance the malignant characteristics of esophageal squamous cell carcinoma by increasing sp1 expression
callnumber	RC254-282
title_auth	Long Noncoding RNA FGD5-AS1 Acts as a Competing Endogenous RNA on microRNA-383 to Enhance the Malignant Characteristics of Esophageal Squamous Cell Carcinoma by Increasing SP1 Expression
abstract	Jia Gao,1,* Ziteng Zhang,2,* Hong Su,1 Ling Zong,2 Yan Li1 1Department of Thoracic Surgery, Heze Municipal Hospital, Heze, Shandong 274031, People’s Republic of China; 2Department of Thoracic Surgery, Affiliated Hospital of Jining Medical University, Shandong 272000, People’s Republic of China*These authors contributed equally to this workCorrespondence: Yan LiDepartment of Thoracic Surgery, Heze Municipal Hospital, No. 2888 Caozhou West Road, Heze, Shandong 274031, People’s Republic of ChinaEmail yanli_heze163.comPurpose: Previous studies have identified the important roles of a long noncoding RNA called FGD5 antisense RNA 1 (FGD5-AS1) in several types of human cancer. Nonetheless, to our knowledge, the expression and functions of FGD5-AS1 in esophageal squamous cell carcinoma (ESCC) have not been clarified. In this study, we aimed to determine the expression status of long noncoding RNA FGD5-AS1 in ESCC, determine its participation in ESCC progression, and uncover the underlying mechanisms.Methods: ESCC tissue samples and paired normal adjacent tissues were collected to quantify FGD5-AS1 expression by reverse-transcription quantitative PCR. The effects of FGD5-AS1 on ESCC cell proliferation, apoptosis, migration, and invasion in vitro as well as tumor growth in vivo were studied using a Cell Counting Kit-8 assay, flow cytometry, Transwell migration and invasion assays, and an in vivo tumor xenograft experiment.Results: FGD5-AS1 was found to be aberrantly upregulated in both ESCC tumors and cell lines compared to the control groups. Increased FGD5-AS1 expression manifested a close association with tumor size, TNM stage, and lymph node metastasis in patients with ESCC. Overall survival of patients with ESCC was shorter in the FGD5-AS1 high-expression group than in the FGD5-AS1 low-expression group. An FGD5-AS1 knockdown markedly attenuated ESCC cell proliferation, migration, and invasion and promoted apoptosis in vitro as well as slowed tumor growth in vivo. Mechanism investigation revealed that FGD5-AS1 can increase SP1 expression by sponging microRNA-383 (miR-383), thus functioning as a competing endogenous RNA. An miR-383 knockdown and recovery of SP1 expression attenuated the inhibition of the malignant characteristics of ESCC cells by the FGD5-AS1 knockdown.Conclusion: Thus, FGD5-AS1 enhances the aggressive phenotype of ESCC cells in vitro and in vivo via the miR-383–SP1 axis, which may represent a novel target for ESCC therapy.Keywords: esophageal squamous cell carcinoma, FGD5 antisense RNA 1, microRNA-383
abstractGer	Jia Gao,1,* Ziteng Zhang,2,* Hong Su,1 Ling Zong,2 Yan Li1 1Department of Thoracic Surgery, Heze Municipal Hospital, Heze, Shandong 274031, People’s Republic of China; 2Department of Thoracic Surgery, Affiliated Hospital of Jining Medical University, Shandong 272000, People’s Republic of China*These authors contributed equally to this workCorrespondence: Yan LiDepartment of Thoracic Surgery, Heze Municipal Hospital, No. 2888 Caozhou West Road, Heze, Shandong 274031, People’s Republic of ChinaEmail yanli_heze163.comPurpose: Previous studies have identified the important roles of a long noncoding RNA called FGD5 antisense RNA 1 (FGD5-AS1) in several types of human cancer. Nonetheless, to our knowledge, the expression and functions of FGD5-AS1 in esophageal squamous cell carcinoma (ESCC) have not been clarified. In this study, we aimed to determine the expression status of long noncoding RNA FGD5-AS1 in ESCC, determine its participation in ESCC progression, and uncover the underlying mechanisms.Methods: ESCC tissue samples and paired normal adjacent tissues were collected to quantify FGD5-AS1 expression by reverse-transcription quantitative PCR. The effects of FGD5-AS1 on ESCC cell proliferation, apoptosis, migration, and invasion in vitro as well as tumor growth in vivo were studied using a Cell Counting Kit-8 assay, flow cytometry, Transwell migration and invasion assays, and an in vivo tumor xenograft experiment.Results: FGD5-AS1 was found to be aberrantly upregulated in both ESCC tumors and cell lines compared to the control groups. Increased FGD5-AS1 expression manifested a close association with tumor size, TNM stage, and lymph node metastasis in patients with ESCC. Overall survival of patients with ESCC was shorter in the FGD5-AS1 high-expression group than in the FGD5-AS1 low-expression group. An FGD5-AS1 knockdown markedly attenuated ESCC cell proliferation, migration, and invasion and promoted apoptosis in vitro as well as slowed tumor growth in vivo. Mechanism investigation revealed that FGD5-AS1 can increase SP1 expression by sponging microRNA-383 (miR-383), thus functioning as a competing endogenous RNA. An miR-383 knockdown and recovery of SP1 expression attenuated the inhibition of the malignant characteristics of ESCC cells by the FGD5-AS1 knockdown.Conclusion: Thus, FGD5-AS1 enhances the aggressive phenotype of ESCC cells in vitro and in vivo via the miR-383–SP1 axis, which may represent a novel target for ESCC therapy.Keywords: esophageal squamous cell carcinoma, FGD5 antisense RNA 1, microRNA-383
abstract_unstemmed	Jia Gao,1,* Ziteng Zhang,2,* Hong Su,1 Ling Zong,2 Yan Li1 1Department of Thoracic Surgery, Heze Municipal Hospital, Heze, Shandong 274031, People’s Republic of China; 2Department of Thoracic Surgery, Affiliated Hospital of Jining Medical University, Shandong 272000, People’s Republic of China*These authors contributed equally to this workCorrespondence: Yan LiDepartment of Thoracic Surgery, Heze Municipal Hospital, No. 2888 Caozhou West Road, Heze, Shandong 274031, People’s Republic of ChinaEmail yanli_heze163.comPurpose: Previous studies have identified the important roles of a long noncoding RNA called FGD5 antisense RNA 1 (FGD5-AS1) in several types of human cancer. Nonetheless, to our knowledge, the expression and functions of FGD5-AS1 in esophageal squamous cell carcinoma (ESCC) have not been clarified. In this study, we aimed to determine the expression status of long noncoding RNA FGD5-AS1 in ESCC, determine its participation in ESCC progression, and uncover the underlying mechanisms.Methods: ESCC tissue samples and paired normal adjacent tissues were collected to quantify FGD5-AS1 expression by reverse-transcription quantitative PCR. The effects of FGD5-AS1 on ESCC cell proliferation, apoptosis, migration, and invasion in vitro as well as tumor growth in vivo were studied using a Cell Counting Kit-8 assay, flow cytometry, Transwell migration and invasion assays, and an in vivo tumor xenograft experiment.Results: FGD5-AS1 was found to be aberrantly upregulated in both ESCC tumors and cell lines compared to the control groups. Increased FGD5-AS1 expression manifested a close association with tumor size, TNM stage, and lymph node metastasis in patients with ESCC. Overall survival of patients with ESCC was shorter in the FGD5-AS1 high-expression group than in the FGD5-AS1 low-expression group. An FGD5-AS1 knockdown markedly attenuated ESCC cell proliferation, migration, and invasion and promoted apoptosis in vitro as well as slowed tumor growth in vivo. Mechanism investigation revealed that FGD5-AS1 can increase SP1 expression by sponging microRNA-383 (miR-383), thus functioning as a competing endogenous RNA. An miR-383 knockdown and recovery of SP1 expression attenuated the inhibition of the malignant characteristics of ESCC cells by the FGD5-AS1 knockdown.Conclusion: Thus, FGD5-AS1 enhances the aggressive phenotype of ESCC cells in vitro and in vivo via the miR-383–SP1 axis, which may represent a novel target for ESCC therapy.Keywords: esophageal squamous cell carcinoma, FGD5 antisense RNA 1, microRNA-383
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title_short	Long Noncoding RNA FGD5-AS1 Acts as a Competing Endogenous RNA on microRNA-383 to Enhance the Malignant Characteristics of Esophageal Squamous Cell Carcinoma by Increasing SP1 Expression
url	https://doaj.org/article/9430d66b84dc4231986cd4fa1a048f1a https://www.dovepress.com/long-noncoding-rna-fgd5-as1-acts-as-a-competing-endogenous-rna-on-micr-peer-reviewed-article-CMAR https://doaj.org/toc/1179-1322
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Increased FGD5-AS1 expression manifested a close association with tumor size, TNM stage, and lymph node metastasis in patients with ESCC. Overall survival of patients with ESCC was shorter in the FGD5-AS1 high-expression group than in the FGD5-AS1 low-expression group. An FGD5-AS1 knockdown markedly attenuated ESCC cell proliferation, migration, and invasion and promoted apoptosis in vitro as well as slowed tumor growth in vivo. Mechanism investigation revealed that FGD5-AS1 can increase SP1 expression by sponging microRNA-383 (miR-383), thus functioning as a competing endogenous RNA. 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Long Noncoding RNA FGD5-AS1 Acts as a Competing Endogenous RNA on microRNA-383 to Enhance the Malignant Characteristics of Esophageal Squamous Cell Carcinoma by Increasing SP1 Expression

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