Hsa_circ_0084912 Drives the Progression of Cervical Cancer Via Regulating miR-429/SOX2 Pathway
Abstract We focus on hsa_circ_0084912’s role in Cervical cancer (CC) and its molecular pathways. In order to determine the expression of Hsa_circ_0084912, miR-429, and SOX2 in CC tissues and cells, Western blotting and quantitative real-time polymerase chain reaction (qRT-PCR) were utilized. Cell co...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Du, Rong [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2023 |
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| Schlagwörter: |
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| Anmerkung: |
© The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. |
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| Übergeordnetes Werk: |
Enthalten in: Molecular biotechnology - New York, NY : Springer, 1994, 65(2023), 12 vom: 13. März, Seite 2018-2029 |
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| Übergeordnetes Werk: |
volume:65 ; year:2023 ; number:12 ; day:13 ; month:03 ; pages:2018-2029 |
| Links: |
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| DOI / URN: |
10.1007/s12033-023-00701-6 |
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| Katalog-ID: |
SPR053638409 |
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| 520 | |a Abstract We focus on hsa_circ_0084912’s role in Cervical cancer (CC) and its molecular pathways. In order to determine the expression of Hsa_circ_0084912, miR-429, and SOX2 in CC tissues and cells, Western blotting and quantitative real-time polymerase chain reaction (qRT-PCR) were utilized. Cell counting kit 8 (CCK-8), colony formation and Transwell assays were respectively to analyze CC cell proliferation viability, clone formation ability and migration. RNA immunoprecipitation (RIP) assay and dual-luciferase assay were used to assure the targeting correlation among hsa_circ_0084912/SOX2 and miR-429. By using a xenograft tumor model, the hsa_circ_0084912 impact on CC cell proliferation in vivo was confirmed. Hsa_circ_0084912 and SOX2 expressions were aggrandized, however, miR-429 expression was descended in CC tissues and cells. Silencing hsa_circ_0084912 inhibited cell proliferation, colony formation and migration in vitro of CC, meanwhile reducing growth of tumor in vivo. MiR-429 might be sponged by Hsa_circ_0084912 to control SOX2 expression. Hsa_circ_0084912 knockdown impact on the malignant phenotypes of CC cells was restored by miR-429 inhibitor. Moreover, SOX2 silencing eliminated the promotive effects of miR-429 inhibitors on CC cell malignancies. By raising SOX2 expression by targeting miR-429, hsa_circ_0084912 accelerated the development of CC, offering fresh proof that it is a viable target for CC treatment. | ||
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10.1007/s12033-023-00701-6 doi (DE-627)SPR053638409 (SPR)s12033-023-00701-6-e DE-627 ger DE-627 rakwb eng Du, Rong verfasserin aut Hsa_circ_0084912 Drives the Progression of Cervical Cancer Via Regulating miR-429/SOX2 Pathway 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Abstract We focus on hsa_circ_0084912’s role in Cervical cancer (CC) and its molecular pathways. In order to determine the expression of Hsa_circ_0084912, miR-429, and SOX2 in CC tissues and cells, Western blotting and quantitative real-time polymerase chain reaction (qRT-PCR) were utilized. Cell counting kit 8 (CCK-8), colony formation and Transwell assays were respectively to analyze CC cell proliferation viability, clone formation ability and migration. RNA immunoprecipitation (RIP) assay and dual-luciferase assay were used to assure the targeting correlation among hsa_circ_0084912/SOX2 and miR-429. By using a xenograft tumor model, the hsa_circ_0084912 impact on CC cell proliferation in vivo was confirmed. Hsa_circ_0084912 and SOX2 expressions were aggrandized, however, miR-429 expression was descended in CC tissues and cells. Silencing hsa_circ_0084912 inhibited cell proliferation, colony formation and migration in vitro of CC, meanwhile reducing growth of tumor in vivo. MiR-429 might be sponged by Hsa_circ_0084912 to control SOX2 expression. Hsa_circ_0084912 knockdown impact on the malignant phenotypes of CC cells was restored by miR-429 inhibitor. Moreover, SOX2 silencing eliminated the promotive effects of miR-429 inhibitors on CC cell malignancies. By raising SOX2 expression by targeting miR-429, hsa_circ_0084912 accelerated the development of CC, offering fresh proof that it is a viable target for CC treatment. circRNA (dpeaa)DE-He213 miRNA (dpeaa)DE-He213 mRNA (dpeaa)DE-He213 Cervical carcinoma (dpeaa)DE-He213 Xiong, Shiyi (orcid)0000-0001-9544-6707 aut Enthalten in Molecular biotechnology New York, NY : Springer, 1994 65(2023), 12 vom: 13. März, Seite 2018-2029 (DE-627)343966271 (DE-600)2073594-7 1559-0305 nnns volume:65 year:2023 number:12 day:13 month:03 pages:2018-2029 https://dx.doi.org/10.1007/s12033-023-00701-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 65 2023 12 13 03 2018-2029 |
| spelling |
10.1007/s12033-023-00701-6 doi (DE-627)SPR053638409 (SPR)s12033-023-00701-6-e DE-627 ger DE-627 rakwb eng Du, Rong verfasserin aut Hsa_circ_0084912 Drives the Progression of Cervical Cancer Via Regulating miR-429/SOX2 Pathway 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Abstract We focus on hsa_circ_0084912’s role in Cervical cancer (CC) and its molecular pathways. In order to determine the expression of Hsa_circ_0084912, miR-429, and SOX2 in CC tissues and cells, Western blotting and quantitative real-time polymerase chain reaction (qRT-PCR) were utilized. Cell counting kit 8 (CCK-8), colony formation and Transwell assays were respectively to analyze CC cell proliferation viability, clone formation ability and migration. RNA immunoprecipitation (RIP) assay and dual-luciferase assay were used to assure the targeting correlation among hsa_circ_0084912/SOX2 and miR-429. By using a xenograft tumor model, the hsa_circ_0084912 impact on CC cell proliferation in vivo was confirmed. Hsa_circ_0084912 and SOX2 expressions were aggrandized, however, miR-429 expression was descended in CC tissues and cells. Silencing hsa_circ_0084912 inhibited cell proliferation, colony formation and migration in vitro of CC, meanwhile reducing growth of tumor in vivo. MiR-429 might be sponged by Hsa_circ_0084912 to control SOX2 expression. Hsa_circ_0084912 knockdown impact on the malignant phenotypes of CC cells was restored by miR-429 inhibitor. Moreover, SOX2 silencing eliminated the promotive effects of miR-429 inhibitors on CC cell malignancies. By raising SOX2 expression by targeting miR-429, hsa_circ_0084912 accelerated the development of CC, offering fresh proof that it is a viable target for CC treatment. circRNA (dpeaa)DE-He213 miRNA (dpeaa)DE-He213 mRNA (dpeaa)DE-He213 Cervical carcinoma (dpeaa)DE-He213 Xiong, Shiyi (orcid)0000-0001-9544-6707 aut Enthalten in Molecular biotechnology New York, NY : Springer, 1994 65(2023), 12 vom: 13. März, Seite 2018-2029 (DE-627)343966271 (DE-600)2073594-7 1559-0305 nnns volume:65 year:2023 number:12 day:13 month:03 pages:2018-2029 https://dx.doi.org/10.1007/s12033-023-00701-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 65 2023 12 13 03 2018-2029 |
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10.1007/s12033-023-00701-6 doi (DE-627)SPR053638409 (SPR)s12033-023-00701-6-e DE-627 ger DE-627 rakwb eng Du, Rong verfasserin aut Hsa_circ_0084912 Drives the Progression of Cervical Cancer Via Regulating miR-429/SOX2 Pathway 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Abstract We focus on hsa_circ_0084912’s role in Cervical cancer (CC) and its molecular pathways. In order to determine the expression of Hsa_circ_0084912, miR-429, and SOX2 in CC tissues and cells, Western blotting and quantitative real-time polymerase chain reaction (qRT-PCR) were utilized. Cell counting kit 8 (CCK-8), colony formation and Transwell assays were respectively to analyze CC cell proliferation viability, clone formation ability and migration. RNA immunoprecipitation (RIP) assay and dual-luciferase assay were used to assure the targeting correlation among hsa_circ_0084912/SOX2 and miR-429. By using a xenograft tumor model, the hsa_circ_0084912 impact on CC cell proliferation in vivo was confirmed. Hsa_circ_0084912 and SOX2 expressions were aggrandized, however, miR-429 expression was descended in CC tissues and cells. Silencing hsa_circ_0084912 inhibited cell proliferation, colony formation and migration in vitro of CC, meanwhile reducing growth of tumor in vivo. MiR-429 might be sponged by Hsa_circ_0084912 to control SOX2 expression. Hsa_circ_0084912 knockdown impact on the malignant phenotypes of CC cells was restored by miR-429 inhibitor. Moreover, SOX2 silencing eliminated the promotive effects of miR-429 inhibitors on CC cell malignancies. By raising SOX2 expression by targeting miR-429, hsa_circ_0084912 accelerated the development of CC, offering fresh proof that it is a viable target for CC treatment. circRNA (dpeaa)DE-He213 miRNA (dpeaa)DE-He213 mRNA (dpeaa)DE-He213 Cervical carcinoma (dpeaa)DE-He213 Xiong, Shiyi (orcid)0000-0001-9544-6707 aut Enthalten in Molecular biotechnology New York, NY : Springer, 1994 65(2023), 12 vom: 13. März, Seite 2018-2029 (DE-627)343966271 (DE-600)2073594-7 1559-0305 nnns volume:65 year:2023 number:12 day:13 month:03 pages:2018-2029 https://dx.doi.org/10.1007/s12033-023-00701-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 65 2023 12 13 03 2018-2029 |
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10.1007/s12033-023-00701-6 doi (DE-627)SPR053638409 (SPR)s12033-023-00701-6-e DE-627 ger DE-627 rakwb eng Du, Rong verfasserin aut Hsa_circ_0084912 Drives the Progression of Cervical Cancer Via Regulating miR-429/SOX2 Pathway 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Abstract We focus on hsa_circ_0084912’s role in Cervical cancer (CC) and its molecular pathways. In order to determine the expression of Hsa_circ_0084912, miR-429, and SOX2 in CC tissues and cells, Western blotting and quantitative real-time polymerase chain reaction (qRT-PCR) were utilized. Cell counting kit 8 (CCK-8), colony formation and Transwell assays were respectively to analyze CC cell proliferation viability, clone formation ability and migration. RNA immunoprecipitation (RIP) assay and dual-luciferase assay were used to assure the targeting correlation among hsa_circ_0084912/SOX2 and miR-429. By using a xenograft tumor model, the hsa_circ_0084912 impact on CC cell proliferation in vivo was confirmed. Hsa_circ_0084912 and SOX2 expressions were aggrandized, however, miR-429 expression was descended in CC tissues and cells. Silencing hsa_circ_0084912 inhibited cell proliferation, colony formation and migration in vitro of CC, meanwhile reducing growth of tumor in vivo. MiR-429 might be sponged by Hsa_circ_0084912 to control SOX2 expression. Hsa_circ_0084912 knockdown impact on the malignant phenotypes of CC cells was restored by miR-429 inhibitor. Moreover, SOX2 silencing eliminated the promotive effects of miR-429 inhibitors on CC cell malignancies. By raising SOX2 expression by targeting miR-429, hsa_circ_0084912 accelerated the development of CC, offering fresh proof that it is a viable target for CC treatment. circRNA (dpeaa)DE-He213 miRNA (dpeaa)DE-He213 mRNA (dpeaa)DE-He213 Cervical carcinoma (dpeaa)DE-He213 Xiong, Shiyi (orcid)0000-0001-9544-6707 aut Enthalten in Molecular biotechnology New York, NY : Springer, 1994 65(2023), 12 vom: 13. März, Seite 2018-2029 (DE-627)343966271 (DE-600)2073594-7 1559-0305 nnns volume:65 year:2023 number:12 day:13 month:03 pages:2018-2029 https://dx.doi.org/10.1007/s12033-023-00701-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 65 2023 12 13 03 2018-2029 |
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10.1007/s12033-023-00701-6 doi (DE-627)SPR053638409 (SPR)s12033-023-00701-6-e DE-627 ger DE-627 rakwb eng Du, Rong verfasserin aut Hsa_circ_0084912 Drives the Progression of Cervical Cancer Via Regulating miR-429/SOX2 Pathway 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Abstract We focus on hsa_circ_0084912’s role in Cervical cancer (CC) and its molecular pathways. In order to determine the expression of Hsa_circ_0084912, miR-429, and SOX2 in CC tissues and cells, Western blotting and quantitative real-time polymerase chain reaction (qRT-PCR) were utilized. Cell counting kit 8 (CCK-8), colony formation and Transwell assays were respectively to analyze CC cell proliferation viability, clone formation ability and migration. RNA immunoprecipitation (RIP) assay and dual-luciferase assay were used to assure the targeting correlation among hsa_circ_0084912/SOX2 and miR-429. By using a xenograft tumor model, the hsa_circ_0084912 impact on CC cell proliferation in vivo was confirmed. Hsa_circ_0084912 and SOX2 expressions were aggrandized, however, miR-429 expression was descended in CC tissues and cells. Silencing hsa_circ_0084912 inhibited cell proliferation, colony formation and migration in vitro of CC, meanwhile reducing growth of tumor in vivo. MiR-429 might be sponged by Hsa_circ_0084912 to control SOX2 expression. Hsa_circ_0084912 knockdown impact on the malignant phenotypes of CC cells was restored by miR-429 inhibitor. Moreover, SOX2 silencing eliminated the promotive effects of miR-429 inhibitors on CC cell malignancies. By raising SOX2 expression by targeting miR-429, hsa_circ_0084912 accelerated the development of CC, offering fresh proof that it is a viable target for CC treatment. circRNA (dpeaa)DE-He213 miRNA (dpeaa)DE-He213 mRNA (dpeaa)DE-He213 Cervical carcinoma (dpeaa)DE-He213 Xiong, Shiyi (orcid)0000-0001-9544-6707 aut Enthalten in Molecular biotechnology New York, NY : Springer, 1994 65(2023), 12 vom: 13. März, Seite 2018-2029 (DE-627)343966271 (DE-600)2073594-7 1559-0305 nnns volume:65 year:2023 number:12 day:13 month:03 pages:2018-2029 https://dx.doi.org/10.1007/s12033-023-00701-6 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 65 2023 12 13 03 2018-2029 |
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Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract We focus on hsa_circ_0084912’s role in Cervical cancer (CC) and its molecular pathways. In order to determine the expression of Hsa_circ_0084912, miR-429, and SOX2 in CC tissues and cells, Western blotting and quantitative real-time polymerase chain reaction (qRT-PCR) were utilized. Cell counting kit 8 (CCK-8), colony formation and Transwell assays were respectively to analyze CC cell proliferation viability, clone formation ability and migration. RNA immunoprecipitation (RIP) assay and dual-luciferase assay were used to assure the targeting correlation among hsa_circ_0084912/SOX2 and miR-429. By using a xenograft tumor model, the hsa_circ_0084912 impact on CC cell proliferation in vivo was confirmed. Hsa_circ_0084912 and SOX2 expressions were aggrandized, however, miR-429 expression was descended in CC tissues and cells. Silencing hsa_circ_0084912 inhibited cell proliferation, colony formation and migration in vitro of CC, meanwhile reducing growth of tumor in vivo. MiR-429 might be sponged by Hsa_circ_0084912 to control SOX2 expression. Hsa_circ_0084912 knockdown impact on the malignant phenotypes of CC cells was restored by miR-429 inhibitor. Moreover, SOX2 silencing eliminated the promotive effects of miR-429 inhibitors on CC cell malignancies. 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Du, Rong |
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Du, Rong misc circRNA misc miRNA misc mRNA misc Cervical carcinoma Hsa_circ_0084912 Drives the Progression of Cervical Cancer Via Regulating miR-429/SOX2 Pathway |
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Hsa_circ_0084912 Drives the Progression of Cervical Cancer Via Regulating miR-429/SOX2 Pathway circRNA (dpeaa)DE-He213 miRNA (dpeaa)DE-He213 mRNA (dpeaa)DE-He213 Cervical carcinoma (dpeaa)DE-He213 |
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hsa_circ_0084912 drives the progression of cervical cancer via regulating mir-429/sox2 pathway |
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Hsa_circ_0084912 Drives the Progression of Cervical Cancer Via Regulating miR-429/SOX2 Pathway |
| abstract |
Abstract We focus on hsa_circ_0084912’s role in Cervical cancer (CC) and its molecular pathways. In order to determine the expression of Hsa_circ_0084912, miR-429, and SOX2 in CC tissues and cells, Western blotting and quantitative real-time polymerase chain reaction (qRT-PCR) were utilized. Cell counting kit 8 (CCK-8), colony formation and Transwell assays were respectively to analyze CC cell proliferation viability, clone formation ability and migration. RNA immunoprecipitation (RIP) assay and dual-luciferase assay were used to assure the targeting correlation among hsa_circ_0084912/SOX2 and miR-429. By using a xenograft tumor model, the hsa_circ_0084912 impact on CC cell proliferation in vivo was confirmed. Hsa_circ_0084912 and SOX2 expressions were aggrandized, however, miR-429 expression was descended in CC tissues and cells. Silencing hsa_circ_0084912 inhibited cell proliferation, colony formation and migration in vitro of CC, meanwhile reducing growth of tumor in vivo. MiR-429 might be sponged by Hsa_circ_0084912 to control SOX2 expression. Hsa_circ_0084912 knockdown impact on the malignant phenotypes of CC cells was restored by miR-429 inhibitor. Moreover, SOX2 silencing eliminated the promotive effects of miR-429 inhibitors on CC cell malignancies. By raising SOX2 expression by targeting miR-429, hsa_circ_0084912 accelerated the development of CC, offering fresh proof that it is a viable target for CC treatment. © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. |
| abstractGer |
Abstract We focus on hsa_circ_0084912’s role in Cervical cancer (CC) and its molecular pathways. In order to determine the expression of Hsa_circ_0084912, miR-429, and SOX2 in CC tissues and cells, Western blotting and quantitative real-time polymerase chain reaction (qRT-PCR) were utilized. Cell counting kit 8 (CCK-8), colony formation and Transwell assays were respectively to analyze CC cell proliferation viability, clone formation ability and migration. RNA immunoprecipitation (RIP) assay and dual-luciferase assay were used to assure the targeting correlation among hsa_circ_0084912/SOX2 and miR-429. By using a xenograft tumor model, the hsa_circ_0084912 impact on CC cell proliferation in vivo was confirmed. Hsa_circ_0084912 and SOX2 expressions were aggrandized, however, miR-429 expression was descended in CC tissues and cells. Silencing hsa_circ_0084912 inhibited cell proliferation, colony formation and migration in vitro of CC, meanwhile reducing growth of tumor in vivo. MiR-429 might be sponged by Hsa_circ_0084912 to control SOX2 expression. Hsa_circ_0084912 knockdown impact on the malignant phenotypes of CC cells was restored by miR-429 inhibitor. Moreover, SOX2 silencing eliminated the promotive effects of miR-429 inhibitors on CC cell malignancies. By raising SOX2 expression by targeting miR-429, hsa_circ_0084912 accelerated the development of CC, offering fresh proof that it is a viable target for CC treatment. © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. |
| abstract_unstemmed |
Abstract We focus on hsa_circ_0084912’s role in Cervical cancer (CC) and its molecular pathways. In order to determine the expression of Hsa_circ_0084912, miR-429, and SOX2 in CC tissues and cells, Western blotting and quantitative real-time polymerase chain reaction (qRT-PCR) were utilized. Cell counting kit 8 (CCK-8), colony formation and Transwell assays were respectively to analyze CC cell proliferation viability, clone formation ability and migration. RNA immunoprecipitation (RIP) assay and dual-luciferase assay were used to assure the targeting correlation among hsa_circ_0084912/SOX2 and miR-429. By using a xenograft tumor model, the hsa_circ_0084912 impact on CC cell proliferation in vivo was confirmed. Hsa_circ_0084912 and SOX2 expressions were aggrandized, however, miR-429 expression was descended in CC tissues and cells. Silencing hsa_circ_0084912 inhibited cell proliferation, colony formation and migration in vitro of CC, meanwhile reducing growth of tumor in vivo. MiR-429 might be sponged by Hsa_circ_0084912 to control SOX2 expression. Hsa_circ_0084912 knockdown impact on the malignant phenotypes of CC cells was restored by miR-429 inhibitor. Moreover, SOX2 silencing eliminated the promotive effects of miR-429 inhibitors on CC cell malignancies. By raising SOX2 expression by targeting miR-429, hsa_circ_0084912 accelerated the development of CC, offering fresh proof that it is a viable target for CC treatment. © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. |
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Hsa_circ_0084912 Drives the Progression of Cervical Cancer Via Regulating miR-429/SOX2 Pathway |
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https://dx.doi.org/10.1007/s12033-023-00701-6 |
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2024-07-03T20:58:02.499Z |
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| score |
7.4019012 |