RNA Binding Motif Protein 3 Promotes Cell Metastasis and Epithelial–Mesenchymal Transition Through STAT3 Signaling Pathway in Hepatocellular Carcinoma

Lu Zhang,1,&ast; Yi Zhang,1,&ast; Dongliang Shen,1 Ying Chen,1 Jianguo Feng,2 Xing Wang,1 Lunkun Ma,1 Yi Liao,3,4 Liling Tang1 1Key Laboratory of Biorheological Science and Technology, Ministry of Education, College of Bioengineering, Chongqing University, Chongqing, 400044, People’s Republic of China; 2Southwest Medical University, Department Anesthesiology, Affiliated Hospital, Luzhou, 646000, People’s Republic of China; 3The Central Laboratory, Shenzhen Second People’s Hospital/First Affiliated Hospital of Shenzhen University Health Science Center, Shenzhen, Guangdong, 518035, People’s Republic of China; 4Department of Thoracic Surgery, Southwest Hospital, Army Medical University, Chongqing, 400038, People’s Republic of China&ast;These authors contributed equally to this workCorrespondence: Liling Tang; Yi Liao, Tel +86 139 9605 1730 ; +86 139 9656 6993, Fax +86-23-65111901 ; +86-23-68763333, Email tanglilingcqu.edu.cn; science0528@163.comPurpose: RNA binding motif protein 3 (RBM3) has been reported to be dysregulated in various cancers and associated with tumor aggressiveness. Epithelial–mesenchymal transition (EMT) is an important biological process by which tumor cells acquire metastatic abilities. This study aimed to explore the regulatory and molecular mechanisms of RBM3 in EMT process.Methods: Western blotting, IHC, and qRT-PCR were performed to evaluate the expression of target genes. Transwell assay was used to investigate the migration and invasion. RNA immunoprecipitation and luciferase reporter assay were performed to explore the correlation of RBM3 with STAT3 or microRNA-383. Animal HCC models were used to explore the role of RBM3 in metastasis in vivo.Results: RBM3 was highly expressed in HCC tissues compared to healthy tissues, and its level was negatively correlated with the prognosis of HCC patients. RBM3 overexpression accelerated migration and invasion, promoted EMT process, and activated STAT3 signaling. EMT induced by RBM3 was not only attenuated by inhibiting pSTAT3 via S3I-201 but also abolished by suppressing STAT3 expression via siRNAs. Mechanistically, RBM3 increased STAT3 expression by stabilizing STAT3 mRNA via binding to its mRNA. As an upstream target of RBM3, microRNA-383 inhibited RBM3 expression by binding to its 3ʹUTR and resulted in the inhibition of the EMT process. Inhibition of RBM3 in HCC animal models prolonged survival and ameliorated malignant phenotypes in mice.Conclusion: Our findings support that RBM3 promotes HCC metastasis by activating STAT3 signaling.Keywords: RBM3, metastasis, EMT, STAT3, microRNA-383 Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Zhang L [verfasserIn] Zhang Y [verfasserIn] Shen D [verfasserIn] Chen Y [verfasserIn] Feng J [verfasserIn] Wang X [verfasserIn] Ma L [verfasserIn] Liao Y [verfasserIn] Tang L [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2022

Schlagwörter:	rbm3 metastasis emt stat3 microrna-383.

Übergeordnetes Werk:	In: Journal of Hepatocellular Carcinoma - Dove Medical Press, 2014, (2022), Seite 405-422
Übergeordnetes Werk:	year:2022 ; pages:405-422

Links:	Link aufrufen Link aufrufen Journal toc

Katalog-ID:	DOAJ041519124

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520			\|a Lu Zhang,1,&ast; Yi Zhang,1,&ast; Dongliang Shen,1 Ying Chen,1 Jianguo Feng,2 Xing Wang,1 Lunkun Ma,1 Yi Liao,3,4 Liling Tang1 1Key Laboratory of Biorheological Science and Technology, Ministry of Education, College of Bioengineering, Chongqing University, Chongqing, 400044, People’s Republic of China; 2Southwest Medical University, Department Anesthesiology, Affiliated Hospital, Luzhou, 646000, People’s Republic of China; 3The Central Laboratory, Shenzhen Second People’s Hospital/First Affiliated Hospital of Shenzhen University Health Science Center, Shenzhen, Guangdong, 518035, People’s Republic of China; 4Department of Thoracic Surgery, Southwest Hospital, Army Medical University, Chongqing, 400038, People’s Republic of China&ast;These authors contributed equally to this workCorrespondence: Liling Tang; Yi Liao, Tel +86 139 9605 1730 ; +86 139 9656 6993, Fax +86-23-65111901 ; +86-23-68763333, Email tanglilingcqu.edu.cn; science0528@163.comPurpose: RNA binding motif protein 3 (RBM3) has been reported to be dysregulated in various cancers and associated with tumor aggressiveness. Epithelial–mesenchymal transition (EMT) is an important biological process by which tumor cells acquire metastatic abilities. This study aimed to explore the regulatory and molecular mechanisms of RBM3 in EMT process.Methods: Western blotting, IHC, and qRT-PCR were performed to evaluate the expression of target genes. Transwell assay was used to investigate the migration and invasion. RNA immunoprecipitation and luciferase reporter assay were performed to explore the correlation of RBM3 with STAT3 or microRNA-383. Animal HCC models were used to explore the role of RBM3 in metastasis in vivo.Results: RBM3 was highly expressed in HCC tissues compared to healthy tissues, and its level was negatively correlated with the prognosis of HCC patients. RBM3 overexpression accelerated migration and invasion, promoted EMT process, and activated STAT3 signaling. EMT induced by RBM3 was not only attenuated by inhibiting pSTAT3 via S3I-201 but also abolished by suppressing STAT3 expression via siRNAs. Mechanistically, RBM3 increased STAT3 expression by stabilizing STAT3 mRNA via binding to its mRNA. As an upstream target of RBM3, microRNA-383 inhibited RBM3 expression by binding to its 3ʹUTR and resulted in the inhibition of the EMT process. Inhibition of RBM3 in HCC animal models prolonged survival and ameliorated malignant phenotypes in mice.Conclusion: Our findings support that RBM3 promotes HCC metastasis by activating STAT3 signaling.Keywords: RBM3, metastasis, EMT, STAT3, microRNA-383
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allfields	(DE-627)DOAJ041519124 (DE-599)DOAJ140802f155094e5fbab91b852f8e1627 DE-627 ger DE-627 rakwb eng RC254-282 Zhang L verfasserin aut RNA Binding Motif Protein 3 Promotes Cell Metastasis and Epithelial–Mesenchymal Transition Through STAT3 Signaling Pathway in Hepatocellular Carcinoma 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Lu Zhang,1,&ast; Yi Zhang,1,&ast; Dongliang Shen,1 Ying Chen,1 Jianguo Feng,2 Xing Wang,1 Lunkun Ma,1 Yi Liao,3,4 Liling Tang1 1Key Laboratory of Biorheological Science and Technology, Ministry of Education, College of Bioengineering, Chongqing University, Chongqing, 400044, People’s Republic of China; 2Southwest Medical University, Department Anesthesiology, Affiliated Hospital, Luzhou, 646000, People’s Republic of China; 3The Central Laboratory, Shenzhen Second People’s Hospital/First Affiliated Hospital of Shenzhen University Health Science Center, Shenzhen, Guangdong, 518035, People’s Republic of China; 4Department of Thoracic Surgery, Southwest Hospital, Army Medical University, Chongqing, 400038, People’s Republic of China&ast;These authors contributed equally to this workCorrespondence: Liling Tang; Yi Liao, Tel +86 139 9605 1730 ; +86 139 9656 6993, Fax +86-23-65111901 ; +86-23-68763333, Email tanglilingcqu.edu.cn; science0528@163.comPurpose: RNA binding motif protein 3 (RBM3) has been reported to be dysregulated in various cancers and associated with tumor aggressiveness. Epithelial–mesenchymal transition (EMT) is an important biological process by which tumor cells acquire metastatic abilities. This study aimed to explore the regulatory and molecular mechanisms of RBM3 in EMT process.Methods: Western blotting, IHC, and qRT-PCR were performed to evaluate the expression of target genes. Transwell assay was used to investigate the migration and invasion. RNA immunoprecipitation and luciferase reporter assay were performed to explore the correlation of RBM3 with STAT3 or microRNA-383. Animal HCC models were used to explore the role of RBM3 in metastasis in vivo.Results: RBM3 was highly expressed in HCC tissues compared to healthy tissues, and its level was negatively correlated with the prognosis of HCC patients. RBM3 overexpression accelerated migration and invasion, promoted EMT process, and activated STAT3 signaling. EMT induced by RBM3 was not only attenuated by inhibiting pSTAT3 via S3I-201 but also abolished by suppressing STAT3 expression via siRNAs. Mechanistically, RBM3 increased STAT3 expression by stabilizing STAT3 mRNA via binding to its mRNA. As an upstream target of RBM3, microRNA-383 inhibited RBM3 expression by binding to its 3ʹUTR and resulted in the inhibition of the EMT process. Inhibition of RBM3 in HCC animal models prolonged survival and ameliorated malignant phenotypes in mice.Conclusion: Our findings support that RBM3 promotes HCC metastasis by activating STAT3 signaling.Keywords: RBM3, metastasis, EMT, STAT3, microRNA-383 rbm3 metastasis emt stat3 microrna-383. Neoplasms. Tumors. Oncology. Including cancer and carcinogens Zhang Y verfasserin aut Shen D verfasserin aut Chen Y verfasserin aut Feng J verfasserin aut Wang X verfasserin aut Ma L verfasserin aut Liao Y verfasserin aut Tang L verfasserin aut In Journal of Hepatocellular Carcinoma Dove Medical Press, 2014 (2022), Seite 405-422 (DE-627)792639324 (DE-600)2780784-8 22535969 nnns year:2022 pages:405-422 https://doaj.org/article/140802f155094e5fbab91b852f8e1627 kostenfrei https://www.dovepress.com/rna-binding-motif-protein-3-promotes-cell-metastasis-and-epithelialmes-peer-reviewed-fulltext-article-JHC kostenfrei https://doaj.org/toc/2253-5969 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA 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_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 2022 405-422
spelling	(DE-627)DOAJ041519124 (DE-599)DOAJ140802f155094e5fbab91b852f8e1627 DE-627 ger DE-627 rakwb eng RC254-282 Zhang L verfasserin aut RNA Binding Motif Protein 3 Promotes Cell Metastasis and Epithelial–Mesenchymal Transition Through STAT3 Signaling Pathway in Hepatocellular Carcinoma 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Lu Zhang,1,&ast; Yi Zhang,1,&ast; Dongliang Shen,1 Ying Chen,1 Jianguo Feng,2 Xing Wang,1 Lunkun Ma,1 Yi Liao,3,4 Liling Tang1 1Key Laboratory of Biorheological Science and Technology, Ministry of Education, College of Bioengineering, Chongqing University, Chongqing, 400044, People’s Republic of China; 2Southwest Medical University, Department Anesthesiology, Affiliated Hospital, Luzhou, 646000, People’s Republic of China; 3The Central Laboratory, Shenzhen Second People’s Hospital/First Affiliated Hospital of Shenzhen University Health Science Center, Shenzhen, Guangdong, 518035, People’s Republic of China; 4Department of Thoracic Surgery, Southwest Hospital, Army Medical University, Chongqing, 400038, People’s Republic of China&ast;These authors contributed equally to this workCorrespondence: Liling Tang; Yi Liao, Tel +86 139 9605 1730 ; +86 139 9656 6993, Fax +86-23-65111901 ; +86-23-68763333, Email tanglilingcqu.edu.cn; science0528@163.comPurpose: RNA binding motif protein 3 (RBM3) has been reported to be dysregulated in various cancers and associated with tumor aggressiveness. Epithelial–mesenchymal transition (EMT) is an important biological process by which tumor cells acquire metastatic abilities. This study aimed to explore the regulatory and molecular mechanisms of RBM3 in EMT process.Methods: Western blotting, IHC, and qRT-PCR were performed to evaluate the expression of target genes. Transwell assay was used to investigate the migration and invasion. RNA immunoprecipitation and luciferase reporter assay were performed to explore the correlation of RBM3 with STAT3 or microRNA-383. Animal HCC models were used to explore the role of RBM3 in metastasis in vivo.Results: RBM3 was highly expressed in HCC tissues compared to healthy tissues, and its level was negatively correlated with the prognosis of HCC patients. RBM3 overexpression accelerated migration and invasion, promoted EMT process, and activated STAT3 signaling. EMT induced by RBM3 was not only attenuated by inhibiting pSTAT3 via S3I-201 but also abolished by suppressing STAT3 expression via siRNAs. Mechanistically, RBM3 increased STAT3 expression by stabilizing STAT3 mRNA via binding to its mRNA. As an upstream target of RBM3, microRNA-383 inhibited RBM3 expression by binding to its 3ʹUTR and resulted in the inhibition of the EMT process. Inhibition of RBM3 in HCC animal models prolonged survival and ameliorated malignant phenotypes in mice.Conclusion: Our findings support that RBM3 promotes HCC metastasis by activating STAT3 signaling.Keywords: RBM3, metastasis, EMT, STAT3, microRNA-383 rbm3 metastasis emt stat3 microrna-383. Neoplasms. Tumors. Oncology. Including cancer and carcinogens Zhang Y verfasserin aut Shen D verfasserin aut Chen Y verfasserin aut Feng J verfasserin aut Wang X verfasserin aut Ma L verfasserin aut Liao Y verfasserin aut Tang L verfasserin aut In Journal of Hepatocellular Carcinoma Dove Medical Press, 2014 (2022), Seite 405-422 (DE-627)792639324 (DE-600)2780784-8 22535969 nnns year:2022 pages:405-422 https://doaj.org/article/140802f155094e5fbab91b852f8e1627 kostenfrei https://www.dovepress.com/rna-binding-motif-protein-3-promotes-cell-metastasis-and-epithelialmes-peer-reviewed-fulltext-article-JHC kostenfrei https://doaj.org/toc/2253-5969 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA 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_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 2022 405-422
allfields_unstemmed	(DE-627)DOAJ041519124 (DE-599)DOAJ140802f155094e5fbab91b852f8e1627 DE-627 ger DE-627 rakwb eng RC254-282 Zhang L verfasserin aut RNA Binding Motif Protein 3 Promotes Cell Metastasis and Epithelial–Mesenchymal Transition Through STAT3 Signaling Pathway in Hepatocellular Carcinoma 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Lu Zhang,1,&ast; Yi Zhang,1,&ast; Dongliang Shen,1 Ying Chen,1 Jianguo Feng,2 Xing Wang,1 Lunkun Ma,1 Yi Liao,3,4 Liling Tang1 1Key Laboratory of Biorheological Science and Technology, Ministry of Education, College of Bioengineering, Chongqing University, Chongqing, 400044, People’s Republic of China; 2Southwest Medical University, Department Anesthesiology, Affiliated Hospital, Luzhou, 646000, People’s Republic of China; 3The Central Laboratory, Shenzhen Second People’s Hospital/First Affiliated Hospital of Shenzhen University Health Science Center, Shenzhen, Guangdong, 518035, People’s Republic of China; 4Department of Thoracic Surgery, Southwest Hospital, Army Medical University, Chongqing, 400038, People’s Republic of China&ast;These authors contributed equally to this workCorrespondence: Liling Tang; Yi Liao, Tel +86 139 9605 1730 ; +86 139 9656 6993, Fax +86-23-65111901 ; +86-23-68763333, Email tanglilingcqu.edu.cn; science0528@163.comPurpose: RNA binding motif protein 3 (RBM3) has been reported to be dysregulated in various cancers and associated with tumor aggressiveness. Epithelial–mesenchymal transition (EMT) is an important biological process by which tumor cells acquire metastatic abilities. This study aimed to explore the regulatory and molecular mechanisms of RBM3 in EMT process.Methods: Western blotting, IHC, and qRT-PCR were performed to evaluate the expression of target genes. Transwell assay was used to investigate the migration and invasion. RNA immunoprecipitation and luciferase reporter assay were performed to explore the correlation of RBM3 with STAT3 or microRNA-383. Animal HCC models were used to explore the role of RBM3 in metastasis in vivo.Results: RBM3 was highly expressed in HCC tissues compared to healthy tissues, and its level was negatively correlated with the prognosis of HCC patients. RBM3 overexpression accelerated migration and invasion, promoted EMT process, and activated STAT3 signaling. EMT induced by RBM3 was not only attenuated by inhibiting pSTAT3 via S3I-201 but also abolished by suppressing STAT3 expression via siRNAs. Mechanistically, RBM3 increased STAT3 expression by stabilizing STAT3 mRNA via binding to its mRNA. As an upstream target of RBM3, microRNA-383 inhibited RBM3 expression by binding to its 3ʹUTR and resulted in the inhibition of the EMT process. Inhibition of RBM3 in HCC animal models prolonged survival and ameliorated malignant phenotypes in mice.Conclusion: Our findings support that RBM3 promotes HCC metastasis by activating STAT3 signaling.Keywords: RBM3, metastasis, EMT, STAT3, microRNA-383 rbm3 metastasis emt stat3 microrna-383. Neoplasms. Tumors. Oncology. Including cancer and carcinogens Zhang Y verfasserin aut Shen D verfasserin aut Chen Y verfasserin aut Feng J verfasserin aut Wang X verfasserin aut Ma L verfasserin aut Liao Y verfasserin aut Tang L verfasserin aut In Journal of Hepatocellular Carcinoma Dove Medical Press, 2014 (2022), Seite 405-422 (DE-627)792639324 (DE-600)2780784-8 22535969 nnns year:2022 pages:405-422 https://doaj.org/article/140802f155094e5fbab91b852f8e1627 kostenfrei https://www.dovepress.com/rna-binding-motif-protein-3-promotes-cell-metastasis-and-epithelialmes-peer-reviewed-fulltext-article-JHC kostenfrei https://doaj.org/toc/2253-5969 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA 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_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 2022 405-422
allfieldsGer	(DE-627)DOAJ041519124 (DE-599)DOAJ140802f155094e5fbab91b852f8e1627 DE-627 ger DE-627 rakwb eng RC254-282 Zhang L verfasserin aut RNA Binding Motif Protein 3 Promotes Cell Metastasis and Epithelial–Mesenchymal Transition Through STAT3 Signaling Pathway in Hepatocellular Carcinoma 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Lu Zhang,1,&ast; Yi Zhang,1,&ast; Dongliang Shen,1 Ying Chen,1 Jianguo Feng,2 Xing Wang,1 Lunkun Ma,1 Yi Liao,3,4 Liling Tang1 1Key Laboratory of Biorheological Science and Technology, Ministry of Education, College of Bioengineering, Chongqing University, Chongqing, 400044, People’s Republic of China; 2Southwest Medical University, Department Anesthesiology, Affiliated Hospital, Luzhou, 646000, People’s Republic of China; 3The Central Laboratory, Shenzhen Second People’s Hospital/First Affiliated Hospital of Shenzhen University Health Science Center, Shenzhen, Guangdong, 518035, People’s Republic of China; 4Department of Thoracic Surgery, Southwest Hospital, Army Medical University, Chongqing, 400038, People’s Republic of China&ast;These authors contributed equally to this workCorrespondence: Liling Tang; Yi Liao, Tel +86 139 9605 1730 ; +86 139 9656 6993, Fax +86-23-65111901 ; +86-23-68763333, Email tanglilingcqu.edu.cn; science0528@163.comPurpose: RNA binding motif protein 3 (RBM3) has been reported to be dysregulated in various cancers and associated with tumor aggressiveness. Epithelial–mesenchymal transition (EMT) is an important biological process by which tumor cells acquire metastatic abilities. This study aimed to explore the regulatory and molecular mechanisms of RBM3 in EMT process.Methods: Western blotting, IHC, and qRT-PCR were performed to evaluate the expression of target genes. Transwell assay was used to investigate the migration and invasion. RNA immunoprecipitation and luciferase reporter assay were performed to explore the correlation of RBM3 with STAT3 or microRNA-383. Animal HCC models were used to explore the role of RBM3 in metastasis in vivo.Results: RBM3 was highly expressed in HCC tissues compared to healthy tissues, and its level was negatively correlated with the prognosis of HCC patients. RBM3 overexpression accelerated migration and invasion, promoted EMT process, and activated STAT3 signaling. EMT induced by RBM3 was not only attenuated by inhibiting pSTAT3 via S3I-201 but also abolished by suppressing STAT3 expression via siRNAs. Mechanistically, RBM3 increased STAT3 expression by stabilizing STAT3 mRNA via binding to its mRNA. As an upstream target of RBM3, microRNA-383 inhibited RBM3 expression by binding to its 3ʹUTR and resulted in the inhibition of the EMT process. Inhibition of RBM3 in HCC animal models prolonged survival and ameliorated malignant phenotypes in mice.Conclusion: Our findings support that RBM3 promotes HCC metastasis by activating STAT3 signaling.Keywords: RBM3, metastasis, EMT, STAT3, microRNA-383 rbm3 metastasis emt stat3 microrna-383. Neoplasms. Tumors. Oncology. Including cancer and carcinogens Zhang Y verfasserin aut Shen D verfasserin aut Chen Y verfasserin aut Feng J verfasserin aut Wang X verfasserin aut Ma L verfasserin aut Liao Y verfasserin aut Tang L verfasserin aut In Journal of Hepatocellular Carcinoma Dove Medical Press, 2014 (2022), Seite 405-422 (DE-627)792639324 (DE-600)2780784-8 22535969 nnns year:2022 pages:405-422 https://doaj.org/article/140802f155094e5fbab91b852f8e1627 kostenfrei https://www.dovepress.com/rna-binding-motif-protein-3-promotes-cell-metastasis-and-epithelialmes-peer-reviewed-fulltext-article-JHC kostenfrei https://doaj.org/toc/2253-5969 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA 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_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 2022 405-422
allfieldsSound	(DE-627)DOAJ041519124 (DE-599)DOAJ140802f155094e5fbab91b852f8e1627 DE-627 ger DE-627 rakwb eng RC254-282 Zhang L verfasserin aut RNA Binding Motif Protein 3 Promotes Cell Metastasis and Epithelial–Mesenchymal Transition Through STAT3 Signaling Pathway in Hepatocellular Carcinoma 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Lu Zhang,1,&ast; Yi Zhang,1,&ast; Dongliang Shen,1 Ying Chen,1 Jianguo Feng,2 Xing Wang,1 Lunkun Ma,1 Yi Liao,3,4 Liling Tang1 1Key Laboratory of Biorheological Science and Technology, Ministry of Education, College of Bioengineering, Chongqing University, Chongqing, 400044, People’s Republic of China; 2Southwest Medical University, Department Anesthesiology, Affiliated Hospital, Luzhou, 646000, People’s Republic of China; 3The Central Laboratory, Shenzhen Second People’s Hospital/First Affiliated Hospital of Shenzhen University Health Science Center, Shenzhen, Guangdong, 518035, People’s Republic of China; 4Department of Thoracic Surgery, Southwest Hospital, Army Medical University, Chongqing, 400038, People’s Republic of China&ast;These authors contributed equally to this workCorrespondence: Liling Tang; Yi Liao, Tel +86 139 9605 1730 ; +86 139 9656 6993, Fax +86-23-65111901 ; +86-23-68763333, Email tanglilingcqu.edu.cn; science0528@163.comPurpose: RNA binding motif protein 3 (RBM3) has been reported to be dysregulated in various cancers and associated with tumor aggressiveness. Epithelial–mesenchymal transition (EMT) is an important biological process by which tumor cells acquire metastatic abilities. This study aimed to explore the regulatory and molecular mechanisms of RBM3 in EMT process.Methods: Western blotting, IHC, and qRT-PCR were performed to evaluate the expression of target genes. Transwell assay was used to investigate the migration and invasion. RNA immunoprecipitation and luciferase reporter assay were performed to explore the correlation of RBM3 with STAT3 or microRNA-383. Animal HCC models were used to explore the role of RBM3 in metastasis in vivo.Results: RBM3 was highly expressed in HCC tissues compared to healthy tissues, and its level was negatively correlated with the prognosis of HCC patients. RBM3 overexpression accelerated migration and invasion, promoted EMT process, and activated STAT3 signaling. EMT induced by RBM3 was not only attenuated by inhibiting pSTAT3 via S3I-201 but also abolished by suppressing STAT3 expression via siRNAs. Mechanistically, RBM3 increased STAT3 expression by stabilizing STAT3 mRNA via binding to its mRNA. As an upstream target of RBM3, microRNA-383 inhibited RBM3 expression by binding to its 3ʹUTR and resulted in the inhibition of the EMT process. Inhibition of RBM3 in HCC animal models prolonged survival and ameliorated malignant phenotypes in mice.Conclusion: Our findings support that RBM3 promotes HCC metastasis by activating STAT3 signaling.Keywords: RBM3, metastasis, EMT, STAT3, microRNA-383 rbm3 metastasis emt stat3 microrna-383. Neoplasms. Tumors. Oncology. Including cancer and carcinogens Zhang Y verfasserin aut Shen D verfasserin aut Chen Y verfasserin aut Feng J verfasserin aut Wang X verfasserin aut Ma L verfasserin aut Liao Y verfasserin aut Tang L verfasserin aut In Journal of Hepatocellular Carcinoma Dove Medical Press, 2014 (2022), Seite 405-422 (DE-627)792639324 (DE-600)2780784-8 22535969 nnns year:2022 pages:405-422 https://doaj.org/article/140802f155094e5fbab91b852f8e1627 kostenfrei https://www.dovepress.com/rna-binding-motif-protein-3-promotes-cell-metastasis-and-epithelialmes-peer-reviewed-fulltext-article-JHC kostenfrei https://doaj.org/toc/2253-5969 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA 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_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 2022 405-422
language	English
source	In Journal of Hepatocellular Carcinoma (2022), Seite 405-422 year:2022 pages:405-422
sourceStr	In Journal of Hepatocellular Carcinoma (2022), Seite 405-422 year:2022 pages:405-422
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	rbm3 metastasis emt stat3 microrna-383. Neoplasms. Tumors. Oncology. Including cancer and carcinogens
isfreeaccess_bool	true
container_title	Journal of Hepatocellular Carcinoma
authorswithroles_txt_mv	Zhang L @@aut@@ Zhang Y @@aut@@ Shen D @@aut@@ Chen Y @@aut@@ Feng J @@aut@@ Wang X @@aut@@ Ma L @@aut@@ Liao Y @@aut@@ Tang L @@aut@@
publishDateDaySort_date	2022-01-01T00:00:00Z
hierarchy_top_id	792639324
id	DOAJ041519124
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">DOAJ041519124</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230502121907.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">230227s2022 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)DOAJ041519124</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)DOAJ140802f155094e5fbab91b852f8e1627</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">Zhang L</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">RNA Binding Motif Protein 3 Promotes Cell Metastasis and Epithelial&ndash;Mesenchymal Transition Through STAT3 Signaling Pathway in Hepatocellular Carcinoma</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2022</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">Lu Zhang,1,&ast; Yi Zhang,1,&ast; Dongliang Shen,1 Ying Chen,1 Jianguo Feng,2 Xing Wang,1 Lunkun Ma,1 Yi Liao,3,4 Liling Tang1 1Key Laboratory of Biorheological Science and Technology, Ministry of Education, College of Bioengineering, Chongqing University, Chongqing, 400044, People’s Republic of China; 2Southwest Medical University, Department Anesthesiology, Affiliated Hospital, Luzhou, 646000, People’s Republic of China; 3The Central Laboratory, Shenzhen Second People’s Hospital/First Affiliated Hospital of Shenzhen University Health Science Center, Shenzhen, Guangdong, 518035, People’s Republic of China; 4Department of Thoracic Surgery, Southwest Hospital, Army Medical University, Chongqing, 400038, People’s Republic of China&ast;These authors contributed equally to this workCorrespondence: Liling Tang; Yi Liao, Tel +86 139 9605 1730 ; +86 139 9656 6993, Fax +86-23-65111901 ; +86-23-68763333, Email tanglilingcqu.edu.cn; science0528@163.comPurpose: RNA binding motif protein 3 (RBM3) has been reported to be dysregulated in various cancers and associated with tumor aggressiveness. Epithelial–mesenchymal transition (EMT) is an important biological process by which tumor cells acquire metastatic abilities. This study aimed to explore the regulatory and molecular mechanisms of RBM3 in EMT process.Methods: Western blotting, IHC, and qRT-PCR were performed to evaluate the expression of target genes. Transwell assay was used to investigate the migration and invasion. RNA immunoprecipitation and luciferase reporter assay were performed to explore the correlation of RBM3 with STAT3 or microRNA-383. Animal HCC models were used to explore the role of RBM3 in metastasis in vivo.Results: RBM3 was highly expressed in HCC tissues compared to healthy tissues, and its level was negatively correlated with the prognosis of HCC patients. RBM3 overexpression accelerated migration and invasion, promoted EMT process, and activated STAT3 signaling. EMT induced by RBM3 was not only attenuated by inhibiting pSTAT3 via S3I-201 but also abolished by suppressing STAT3 expression via siRNAs. Mechanistically, RBM3 increased STAT3 expression by stabilizing STAT3 mRNA via binding to its mRNA. As an upstream target of RBM3, microRNA-383 inhibited RBM3 expression by binding to its 3ʹUTR and resulted in the inhibition of the EMT process. 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callnumber-first	R - Medicine
author	Zhang L
spellingShingle	Zhang L misc RC254-282 misc rbm3 misc metastasis misc emt misc stat3 misc microrna-383. misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens RNA Binding Motif Protein 3 Promotes Cell Metastasis and Epithelial–Mesenchymal Transition Through STAT3 Signaling Pathway in Hepatocellular Carcinoma
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topic_title	RC254-282 RNA Binding Motif Protein 3 Promotes Cell Metastasis and Epithelial–Mesenchymal Transition Through STAT3 Signaling Pathway in Hepatocellular Carcinoma rbm3 metastasis emt stat3 microrna-383
topic	misc RC254-282 misc rbm3 misc metastasis misc emt misc stat3 misc microrna-383. misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens
topic_unstemmed	misc RC254-282 misc rbm3 misc metastasis misc emt misc stat3 misc microrna-383. misc Neoplasms. Tumors. Oncology. Including cancer and carcinogens
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title	RNA Binding Motif Protein 3 Promotes Cell Metastasis and Epithelial–Mesenchymal Transition Through STAT3 Signaling Pathway in Hepatocellular Carcinoma
ctrlnum	(DE-627)DOAJ041519124 (DE-599)DOAJ140802f155094e5fbab91b852f8e1627
title_full	RNA Binding Motif Protein 3 Promotes Cell Metastasis and Epithelial–Mesenchymal Transition Through STAT3 Signaling Pathway in Hepatocellular Carcinoma
author_sort	Zhang L
journal	Journal of Hepatocellular Carcinoma
journalStr	Journal of Hepatocellular Carcinoma
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author_browse	Zhang L Zhang Y Shen D Chen Y Feng J Wang X Ma L Liao Y Tang L
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author-letter	Zhang L
author2-role	verfasserin
title_sort	rna binding motif protein 3 promotes cell metastasis and epithelial–mesenchymal transition through stat3 signaling pathway in hepatocellular carcinoma
callnumber	RC254-282
title_auth	RNA Binding Motif Protein 3 Promotes Cell Metastasis and Epithelial–Mesenchymal Transition Through STAT3 Signaling Pathway in Hepatocellular Carcinoma
abstract	Lu Zhang,1,&ast; Yi Zhang,1,&ast; Dongliang Shen,1 Ying Chen,1 Jianguo Feng,2 Xing Wang,1 Lunkun Ma,1 Yi Liao,3,4 Liling Tang1 1Key Laboratory of Biorheological Science and Technology, Ministry of Education, College of Bioengineering, Chongqing University, Chongqing, 400044, People’s Republic of China; 2Southwest Medical University, Department Anesthesiology, Affiliated Hospital, Luzhou, 646000, People’s Republic of China; 3The Central Laboratory, Shenzhen Second People’s Hospital/First Affiliated Hospital of Shenzhen University Health Science Center, Shenzhen, Guangdong, 518035, People’s Republic of China; 4Department of Thoracic Surgery, Southwest Hospital, Army Medical University, Chongqing, 400038, People’s Republic of China&ast;These authors contributed equally to this workCorrespondence: Liling Tang; Yi Liao, Tel +86 139 9605 1730 ; +86 139 9656 6993, Fax +86-23-65111901 ; +86-23-68763333, Email tanglilingcqu.edu.cn; science0528@163.comPurpose: RNA binding motif protein 3 (RBM3) has been reported to be dysregulated in various cancers and associated with tumor aggressiveness. Epithelial–mesenchymal transition (EMT) is an important biological process by which tumor cells acquire metastatic abilities. This study aimed to explore the regulatory and molecular mechanisms of RBM3 in EMT process.Methods: Western blotting, IHC, and qRT-PCR were performed to evaluate the expression of target genes. Transwell assay was used to investigate the migration and invasion. RNA immunoprecipitation and luciferase reporter assay were performed to explore the correlation of RBM3 with STAT3 or microRNA-383. Animal HCC models were used to explore the role of RBM3 in metastasis in vivo.Results: RBM3 was highly expressed in HCC tissues compared to healthy tissues, and its level was negatively correlated with the prognosis of HCC patients. RBM3 overexpression accelerated migration and invasion, promoted EMT process, and activated STAT3 signaling. EMT induced by RBM3 was not only attenuated by inhibiting pSTAT3 via S3I-201 but also abolished by suppressing STAT3 expression via siRNAs. Mechanistically, RBM3 increased STAT3 expression by stabilizing STAT3 mRNA via binding to its mRNA. As an upstream target of RBM3, microRNA-383 inhibited RBM3 expression by binding to its 3ʹUTR and resulted in the inhibition of the EMT process. Inhibition of RBM3 in HCC animal models prolonged survival and ameliorated malignant phenotypes in mice.Conclusion: Our findings support that RBM3 promotes HCC metastasis by activating STAT3 signaling.Keywords: RBM3, metastasis, EMT, STAT3, microRNA-383
abstractGer	Lu Zhang,1,&ast; Yi Zhang,1,&ast; Dongliang Shen,1 Ying Chen,1 Jianguo Feng,2 Xing Wang,1 Lunkun Ma,1 Yi Liao,3,4 Liling Tang1 1Key Laboratory of Biorheological Science and Technology, Ministry of Education, College of Bioengineering, Chongqing University, Chongqing, 400044, People’s Republic of China; 2Southwest Medical University, Department Anesthesiology, Affiliated Hospital, Luzhou, 646000, People’s Republic of China; 3The Central Laboratory, Shenzhen Second People’s Hospital/First Affiliated Hospital of Shenzhen University Health Science Center, Shenzhen, Guangdong, 518035, People’s Republic of China; 4Department of Thoracic Surgery, Southwest Hospital, Army Medical University, Chongqing, 400038, People’s Republic of China&ast;These authors contributed equally to this workCorrespondence: Liling Tang; Yi Liao, Tel +86 139 9605 1730 ; +86 139 9656 6993, Fax +86-23-65111901 ; +86-23-68763333, Email tanglilingcqu.edu.cn; science0528@163.comPurpose: RNA binding motif protein 3 (RBM3) has been reported to be dysregulated in various cancers and associated with tumor aggressiveness. Epithelial–mesenchymal transition (EMT) is an important biological process by which tumor cells acquire metastatic abilities. This study aimed to explore the regulatory and molecular mechanisms of RBM3 in EMT process.Methods: Western blotting, IHC, and qRT-PCR were performed to evaluate the expression of target genes. Transwell assay was used to investigate the migration and invasion. RNA immunoprecipitation and luciferase reporter assay were performed to explore the correlation of RBM3 with STAT3 or microRNA-383. Animal HCC models were used to explore the role of RBM3 in metastasis in vivo.Results: RBM3 was highly expressed in HCC tissues compared to healthy tissues, and its level was negatively correlated with the prognosis of HCC patients. RBM3 overexpression accelerated migration and invasion, promoted EMT process, and activated STAT3 signaling. EMT induced by RBM3 was not only attenuated by inhibiting pSTAT3 via S3I-201 but also abolished by suppressing STAT3 expression via siRNAs. Mechanistically, RBM3 increased STAT3 expression by stabilizing STAT3 mRNA via binding to its mRNA. As an upstream target of RBM3, microRNA-383 inhibited RBM3 expression by binding to its 3ʹUTR and resulted in the inhibition of the EMT process. Inhibition of RBM3 in HCC animal models prolonged survival and ameliorated malignant phenotypes in mice.Conclusion: Our findings support that RBM3 promotes HCC metastasis by activating STAT3 signaling.Keywords: RBM3, metastasis, EMT, STAT3, microRNA-383
abstract_unstemmed	Lu Zhang,1,&ast; Yi Zhang,1,&ast; Dongliang Shen,1 Ying Chen,1 Jianguo Feng,2 Xing Wang,1 Lunkun Ma,1 Yi Liao,3,4 Liling Tang1 1Key Laboratory of Biorheological Science and Technology, Ministry of Education, College of Bioengineering, Chongqing University, Chongqing, 400044, People’s Republic of China; 2Southwest Medical University, Department Anesthesiology, Affiliated Hospital, Luzhou, 646000, People’s Republic of China; 3The Central Laboratory, Shenzhen Second People’s Hospital/First Affiliated Hospital of Shenzhen University Health Science Center, Shenzhen, Guangdong, 518035, People’s Republic of China; 4Department of Thoracic Surgery, Southwest Hospital, Army Medical University, Chongqing, 400038, People’s Republic of China&ast;These authors contributed equally to this workCorrespondence: Liling Tang; Yi Liao, Tel +86 139 9605 1730 ; +86 139 9656 6993, Fax +86-23-65111901 ; +86-23-68763333, Email tanglilingcqu.edu.cn; science0528@163.comPurpose: RNA binding motif protein 3 (RBM3) has been reported to be dysregulated in various cancers and associated with tumor aggressiveness. Epithelial–mesenchymal transition (EMT) is an important biological process by which tumor cells acquire metastatic abilities. This study aimed to explore the regulatory and molecular mechanisms of RBM3 in EMT process.Methods: Western blotting, IHC, and qRT-PCR were performed to evaluate the expression of target genes. Transwell assay was used to investigate the migration and invasion. RNA immunoprecipitation and luciferase reporter assay were performed to explore the correlation of RBM3 with STAT3 or microRNA-383. Animal HCC models were used to explore the role of RBM3 in metastasis in vivo.Results: RBM3 was highly expressed in HCC tissues compared to healthy tissues, and its level was negatively correlated with the prognosis of HCC patients. RBM3 overexpression accelerated migration and invasion, promoted EMT process, and activated STAT3 signaling. EMT induced by RBM3 was not only attenuated by inhibiting pSTAT3 via S3I-201 but also abolished by suppressing STAT3 expression via siRNAs. Mechanistically, RBM3 increased STAT3 expression by stabilizing STAT3 mRNA via binding to its mRNA. As an upstream target of RBM3, microRNA-383 inhibited RBM3 expression by binding to its 3ʹUTR and resulted in the inhibition of the EMT process. Inhibition of RBM3 in HCC animal models prolonged survival and ameliorated malignant phenotypes in mice.Conclusion: Our findings support that RBM3 promotes HCC metastasis by activating STAT3 signaling.Keywords: RBM3, metastasis, EMT, STAT3, microRNA-383
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title_short	RNA Binding Motif Protein 3 Promotes Cell Metastasis and Epithelial–Mesenchymal Transition Through STAT3 Signaling Pathway in Hepatocellular Carcinoma
url	https://doaj.org/article/140802f155094e5fbab91b852f8e1627 https://www.dovepress.com/rna-binding-motif-protein-3-promotes-cell-metastasis-and-epithelialmes-peer-reviewed-fulltext-article-JHC https://doaj.org/toc/2253-5969
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up_date	2024-07-03T20:41:05.734Z
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RNA Binding Motif Protein 3 Promotes Cell Metastasis and Epithelial&ndash;Mesenchymal Transition Through STAT3 Signaling Pathway in Hepatocellular Carcinoma

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RNA Binding Motif Protein 3 Promotes Cell Metastasis and Epithelial–Mesenchymal Transition Through STAT3 Signaling Pathway in Hepatocellular Carcinoma