BCL6B suppresses proliferation and migration of colorectal carcinoma cells through inhibition of the PI3K/AKT signaling pathway
| Autor: | Xueru Li, Yue Gu, Jia-qing Xie, Ai-fang Li, He Zha, Jia-li Zhao, Hui Sun, Lan Zhou, Zongyue Zeng |
|---|---|
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
proliferation Down-Regulation colorectal cancer migration Phosphatidylinositol 3-Kinases 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Downregulation and upregulation Cell Movement Cell Line Tumor Genetics Humans LY294002 B-cell CLL/lymphoma 6 member B Protein kinase B PI3K/AKT/mTOR pathway Cell Proliferation Phosphoinositide 3-kinase biology Cell growth Articles General Medicine Cell cycle digestive system diseases Gene Expression Regulation Neoplastic Repressor Proteins 030104 developmental biology chemistry 030220 oncology & carcinogenesis biology.protein Cancer research Signal transduction Colorectal Neoplasms phosphoinositide 3 kinase/AKT signaling pathway Proto-Oncogene Proteins c-akt Signal Transduction |
| Zdroj: | International Journal of Molecular Medicine |
| ISSN: | 1791-244X 1107-3756 |
| DOI: | 10.3892/ijmm.2018.3451 |
| Popis: | B-cell CLL/lymphoma 6 member B (BCL6B), a BCL6-homologous gene, has been reported to be a tumor suppressor that is silenced in a variety of human cancers, including colorectal cancer (CRC). Although it was recently demonstrated that reduced expression of BCL6B is associated with tumor stage and lymph node metastasis in CRC, little is known on whether BCL6B contributes to CRC development, or the related underlying mechanism. The aim of the present study was to detect BCL6B expression in CRC cells, and determine the molecular mechanisms underlying the role of BCL6B in CRC development by investigating cell proliferation and migration in vitro. As a result, BCL6B expression was found to be notably repressed in CRC cells compared with normal intestinal epithelial cells by reverse transcription-polymerase chain reaction and western blot analysis. CRC cell proliferation was significantly inhibited by BCL6B upregulation, as indicated by MTT and colony-forming assays. Cell apoptosis was markedly induced, as indicated by flow cytometry, and BCL6B-transfected CRC cells exhibited decreased migration ability. Additionally, BCL6B overexpression diminished the phosphorylation level of AKT in CRC cells. These effects of BCL6B were empowered by treatment with the specific phosphoinositide 3 kinase (PI3K)/AKT inhibitor LY294002. Furthermore, overexpression of BCL6B resulted in upregulation of E-cadherin and downregulation of cyclin D1 and matrix metalloproteinase-9, which were strongly enhanced by LY294002. In conclusion, the findings of the present study demonstrated that BCL6B suppressed the proliferation and migration of CRC cells indirectly, via inhibition of PI3K. |
| Databáze: | OpenAIRE |
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