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Sox2 is involved in paclitaxel resistance of the prostate cancer cell line PC-3 via the PI3K/Akt pathway
- Source :
- Molecular medicine reports. 10(6)
- Publication Year :
- 2013
-
Abstract
- 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.
- Subjects :
- Oncology
Male
Cancer Research
medicine.medical_specialty
Paclitaxel
Survivin
Apoptosis
Biology
medicine.disease_cause
Biochemistry
Inhibitor of Apoptosis Proteins
S Phase
Prostate cancer
Phosphatidylinositol 3-Kinases
SOX2
Internal medicine
Cell Line, Tumor
Cyclin E
Genetics
medicine
Humans
Molecular Biology
PI3K/AKT/mTOR pathway
Cell Proliferation
Akt/PKB signaling pathway
SOXB1 Transcription Factors
G1 Phase
Cancer
Prostatic Neoplasms
Cell cycle
medicine.disease
Drug Resistance, Neoplasm
Molecular Medicine
Carcinogenesis
Proto-Oncogene Proteins c-akt
Signal Transduction
Subjects
Details
- ISSN :
- 17913004
- Volume :
- 10
- Issue :
- 6
- Database :
- OpenAIRE
- Journal :
- Molecular medicine reports
- Accession number :
- edsair.doi.dedup.....1def3974e78bb2c6d7bb4a2df32f7044