IMR Press / EJGO / Volume 36 / Issue 6 / DOI: 10.12892/ejgo2725.2015

European Journal of Gynaecological Oncology (EJGO) is published by IMR Press from Volume 40 Issue 1 (2019). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with S.O.G.

Open Access Original Research
Cytoplasmic p21 is responsible for paclitaxel resistance in ovarian cancer A2780 cells
X. Xia1,2,3T. Ji3R. Liu3Y. Weng3Y. Fang3Z. Wang2H. Xu4,*
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1 Department of Reproductive Center, Peking University Shenzhen Hospital, Shenzhen
2 Department of Gynecology & Obstetrics, Nanshan People's Hospital, Guangdong Medical College, Shenzhen
3 Cancer Biology Research Center, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan
4 Department of Gynecology & Obstetrics, Shenzhen People's Hospital, Second Clinical Medical College, Jinan University, Shenzhen (China)
Eur. J. Gynaecol. Oncol. 2015, 36(6), 662–666; https://doi.org/10.12892/ejgo2725.2015
Published: 10 December 2015
Abstract

Purpose: P21 which bound to cyclin-dependent kinase complexes was originally described as a suppressor of cancer cell proliferation, while many recent studies have shown p21, when accumulated in the cell cytoplasm, could promote tumor progression. This study was conducted to investigate the role of p21 in the paclitaxel (PTX) resistance of ovarian cancer. Materials and Methods: Regulation of cytoplasmic p21 was performed through transfection of Akt2 constitutively active vector, Akt2 shRNA and p21 siRNA in the ovarian cancer cell line A2780. Akt2, p-Akt, and p21 expression were examined by Western blot and cell apoptosis rates were assessed by flow cytometry after treatment with PTX. Results: Induction of p21 translocation into the cytoplasm via constitutively active Akt2 transfection in A2780 enhanced the resistance to PTX, while inhibition of p21 translocation into the cytoplasm via Akt2 shRNA transfection in A2780 cells significantly increased PTX treatment sensitivity. Furthermore, knockdown of cytoplasmic p21 by direct p21 siRNA transfection in Akt2 overexpressed A2780 cells notably increased PTX-induced apoptosis. Conclusion: Cytoplasmic p21 may represent a potential therapeutic target for ovarian tumors that are resistant to PTX treatment.
Keywords
Cytoplasmic p21
PTX resistance
Drug resistance
Ovarian cancer
Akt2
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