Sox2 is involved in paclitaxel resistance of the prostate cancer cell line PC-3 via the PI3K/Akt pathway
Prostate cancer is the most commonly diagnosed type of cancer and the second leading cause of cancer-associated mortality in males. The efficacy of prostate cancer chemotherapy is frequently impaired by drug resistance; however, the underlying mechanisms of this resistance remain elusive. Sex determ...
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Published in | Molecular medicine reports Vol. 10; no. 6; pp. 3169 - 3176 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Greece
D.A. Spandidos
01.12.2014
Spandidos Publications Spandidos Publications UK Ltd |
Subjects | |
Online Access | Get full text |
ISSN | 1791-2997 1791-3004 1791-3004 |
DOI | 10.3892/mmr.2014.2630 |
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Summary: | Prostate cancer is the most commonly diagnosed type of cancer and the second leading cause of cancer-associated mortality in males. The efficacy of prostate cancer chemotherapy is frequently impaired by drug resistance; however, the underlying mechanisms of this resistance remain elusive. Sex determining region Y-box 2 (Sox2) is of vital importance in the regulation of stem cell proliferation and carcinogenesis. In the present study, using MTT, clone formation, cell cycle and apoptosis assays, over-expression of Sox2 was demonstrated to enhance the paclitaxel (Pac) resistance of the PC-3 prostate cancer cell line, promoting cell proliferation and exhibiting an anti-apoptotic effect. Western blot analysis revealed that the phosphoinositide 3-kinase/Akt signaling pathway was activated in cells overexpressing Sox2, and by targeting cyclin E and survivin, Sox2 promoted G1/S phase transition and prevented apoptosis under Pac treatment. The present study provided an understanding of Pac resistance in prostate cancer and may indicate novel therapeutic methods for chemoresistant prostate cancer. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 |
ISSN: | 1791-2997 1791-3004 1791-3004 |
DOI: | 10.3892/mmr.2014.2630 |