MiR-429 Induces Gastric Carcinoma Cell Apoptosis Through Bcl-2
Background/Aims: MicroRNAs (miRNAs) play an essential role in the tumorigenesis of gastric carcinoma (GC). MiR-429 has been recently reported to inhibit GC growth, but the underlying mechanisms are not clear. Methods: Here, we studied the levels of miR-429 and anti-apoptotic protein Bcl-2 in GC spec...
| Main Authors: | , , , , , |
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| Format: | Article |
| Language: | English |
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Cell Physiol Biochem Press GmbH & Co KG
2015-10-01
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| Series: | Cellular Physiology and Biochemistry |
| Subjects: | |
| Online Access: | http://www.karger.com/Article/FullText/438524 |
| _version_ | 1819085778951602176 |
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| author | Ping Zhu Jingping Zhang Jianfei Zhu Jun Shi Qiuwei Zhu Yuanyuan Gao |
| author_facet | Ping Zhu Jingping Zhang Jianfei Zhu Jun Shi Qiuwei Zhu Yuanyuan Gao |
| author_sort | Ping Zhu |
| collection | DOAJ |
| description | Background/Aims: MicroRNAs (miRNAs) play an essential role in the tumorigenesis of gastric carcinoma (GC). MiR-429 has been recently reported to inhibit GC growth, but the underlying mechanisms are not clear. Methods: Here, we studied the levels of miR-429 and anti-apoptotic protein Bcl-2 in GC specimens. We performed bioinformatics analyses and used luciferase-reporter assay to analyze the relationship between miR-429 and Bcl-2 in GC cells. Cell survival upon Fluorouracil treatment was analyzed in a CCK assay. Cell apoptosis was measured by flow cytometry based FITC Annexin V apoptosis detection assay. Results: MiR-429 levels were significantly decreased and Bcl-2 levels were significantly increased in GC specimens, compared to the paired adjacent non-tumor gastric tissue. Moreover, the levels of miR-429 and Bcl-2 inversely correlated in GC specimens. MiR-429-low subjects had an overall inferior survival, compared to miR-429-high subjects. Bioinformatics analyses showed that miR-429 targeted the 3'-UTR of Bcl-2 mRNA to inhibit its translation, which was confirmed by luciferase-reporter assay. Overexpression of miR-429 inhibited Bcl-2-mediated cell survival against apoptosis induced by Fluorouracil, while depletion of miR-429 augmented it. Conclusion: Our data suggest that miR-429 suppression in GC promotes Bcl-2-mediated cancer cell survival against chemotherapy-induced cell death. Re-expression of miR-429 levels in GC cells may enhance cancer apoptosis during chemotherapy. |
| first_indexed | 2024-12-21T21:09:46Z |
| format | Article |
| id | doaj.art-a2116b2d69d74eb1b66fa1b716a552fa |
| institution | Directory Open Access Journal |
| issn | 1015-8987 1421-9778 |
| language | English |
| last_indexed | 2024-12-21T21:09:46Z |
| publishDate | 2015-10-01 |
| publisher | Cell Physiol Biochem Press GmbH & Co KG |
| record_format | Article |
| series | Cellular Physiology and Biochemistry |
| spelling | doaj.art-a2116b2d69d74eb1b66fa1b716a552fa2022-12-21T18:50:11ZengCell Physiol Biochem Press GmbH & Co KGCellular Physiology and Biochemistry1015-89871421-97782015-10-013741572158010.1159/000438524438524MiR-429 Induces Gastric Carcinoma Cell Apoptosis Through Bcl-2Ping ZhuJingping ZhangJianfei ZhuJun ShiQiuwei ZhuYuanyuan GaoBackground/Aims: MicroRNAs (miRNAs) play an essential role in the tumorigenesis of gastric carcinoma (GC). MiR-429 has been recently reported to inhibit GC growth, but the underlying mechanisms are not clear. Methods: Here, we studied the levels of miR-429 and anti-apoptotic protein Bcl-2 in GC specimens. We performed bioinformatics analyses and used luciferase-reporter assay to analyze the relationship between miR-429 and Bcl-2 in GC cells. Cell survival upon Fluorouracil treatment was analyzed in a CCK assay. Cell apoptosis was measured by flow cytometry based FITC Annexin V apoptosis detection assay. Results: MiR-429 levels were significantly decreased and Bcl-2 levels were significantly increased in GC specimens, compared to the paired adjacent non-tumor gastric tissue. Moreover, the levels of miR-429 and Bcl-2 inversely correlated in GC specimens. MiR-429-low subjects had an overall inferior survival, compared to miR-429-high subjects. Bioinformatics analyses showed that miR-429 targeted the 3'-UTR of Bcl-2 mRNA to inhibit its translation, which was confirmed by luciferase-reporter assay. Overexpression of miR-429 inhibited Bcl-2-mediated cell survival against apoptosis induced by Fluorouracil, while depletion of miR-429 augmented it. Conclusion: Our data suggest that miR-429 suppression in GC promotes Bcl-2-mediated cancer cell survival against chemotherapy-induced cell death. Re-expression of miR-429 levels in GC cells may enhance cancer apoptosis during chemotherapy.http://www.karger.com/Article/FullText/438524ChemotherapyGastric carcinoma (GC)Bcl-2MiR-429 |
| spellingShingle | Ping Zhu Jingping Zhang Jianfei Zhu Jun Shi Qiuwei Zhu Yuanyuan Gao MiR-429 Induces Gastric Carcinoma Cell Apoptosis Through Bcl-2 Cellular Physiology and Biochemistry Chemotherapy Gastric carcinoma (GC) Bcl-2 MiR-429 |
| title | MiR-429 Induces Gastric Carcinoma Cell Apoptosis Through Bcl-2 |
| title_full | MiR-429 Induces Gastric Carcinoma Cell Apoptosis Through Bcl-2 |
| title_fullStr | MiR-429 Induces Gastric Carcinoma Cell Apoptosis Through Bcl-2 |
| title_full_unstemmed | MiR-429 Induces Gastric Carcinoma Cell Apoptosis Through Bcl-2 |
| title_short | MiR-429 Induces Gastric Carcinoma Cell Apoptosis Through Bcl-2 |
| title_sort | mir 429 induces gastric carcinoma cell apoptosis through bcl 2 |
| topic | Chemotherapy Gastric carcinoma (GC) Bcl-2 MiR-429 |
| url | http://www.karger.com/Article/FullText/438524 |
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