Androgen receptor transcriptional activity and chromatin modifications on the ABCB1/MDR gene are critical for taxol resistance in ovarian cancer cells

2018 ◽  
Vol 234 (6) ◽  
pp. 8760-8775 ◽  
Author(s):  
Nian‐Kang Sun ◽  
Abhidha Kohli ◽  
Shang‐Lang Huang ◽  
Ting‐Chang Chang ◽  
Chuck C.‐K. Chao
Keyword(s):  
Ovarian Cancer ◽  
Androgen Receptor ◽  
Cancer Cells ◽  
Transcriptional Activity ◽  
Ovarian Cancer Cells ◽  
Chromatin Modifications ◽  
Taxol Resistance

Increased androgen receptor levels and signaling in ovarian cancer cells by VEPH1 associated with suppression of SMAD3 and AKT activation

2020 ◽  
Vol 196 ◽  
pp. 105498 ◽  
Author(s):  
Alexandra Kollara ◽  
Premalatha Shathasivam ◽  
Soyeon Park ◽  
Maurice J. Ringuette ◽  
Theodore J. Brown
Keyword(s):  
Ovarian Cancer ◽  
Androgen Receptor ◽  
Cancer Cells ◽  
Ovarian Cancer Cells ◽  
Akt Activation

Role of the TLR4-androgen receptor axis and genistein in taxol-resistant ovarian cancer cells

2020 ◽  
Vol 177 ◽  
pp. 113965
Author(s):  
Shang-Lang Huang ◽  
Ting-Chang Chang ◽  
Chuck C.K. Chao ◽  
Nian-Kang Sun
Keyword(s):  
Ovarian Cancer ◽  
Androgen Receptor ◽  
Cancer Cells ◽  
Ovarian Cancer Cells

scholarly journals Carboplatin and taxol resistance develops more rapidly in functional BRCA1 compared to dysfunctional BRCA1 ovarian cancer cells

2015 ◽  
Vol 336 (1) ◽  
pp. 1-14 ◽  
Author(s):  
Steven Busschots ◽  
Sharon O’Toole ◽  
John J. O’Leary ◽  
Britta Stordal
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Ovarian Cancer Cells ◽  
Taxol Resistance

scholarly journals Physapubescin B inhibits tumorgenesis and circumvents taxol resistance of ovarian cancer cells through STAT3 signaling

Oncotarget ◽  
2017 ◽  
Vol 8 (41) ◽  
pp. 70130-70141 ◽  
Author(s):  
Xiaofeng Zhao ◽  
Lu Huang ◽  
Wanwan Xu ◽  
Xiaoyan Chen ◽  
Yan Shen ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Ovarian Cancer Cells ◽  
Stat3 Signaling ◽  
Taxol Resistance

scholarly journals Heat Shock Protein 90 Triggers Multi-Drug Resistance of Ovarian Cancer via AKT/GSK3β/β-Catenin Signaling

2021 ◽  
Vol 11 ◽  
Author(s):  
Lan Yin ◽  
Yuhan Yang ◽  
Wanglong Zhu ◽  
Yu Xian ◽  
Zhengyu Han ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Drug Resistance ◽  
Heat Shock ◽  
Cancer Cells ◽  
Transcriptional Activity ◽  
Heat Shock Protein 90 ◽  
Multi Drug Resistance ◽  
Ovarian Cancer Cells ◽  
Drug Resistant ◽  
Resistance Protein

Ovarian cancer is the most lethal gynaecologic tumor, with which multi-drug resistance as the major therapeutic hindrance. Heat shock protein 90 (Hsp90) has been involved in cancer malignant behaviors. However, its role and mechanism in multi-drug resistance of ovarian cancer remains poorly understood. Our results demonstrated that Hsp90 was overexpressed in multi-drug resistant ovarian cancer cells. Hsp90 downregulation by shHsp90 or inhibitor BIIB021 increased the sensitivity of multi-drug resistant ovarian cancer cells to paclitaxel and cisplatin, and augmented the drugs-induced apoptosis. Hsp90 positively regulated the expressions of multi-drug resistance protein 1 (P-gp/MDR1), breast cancer resistance protein (BCRP), Survivin and Bcl-2 expressions closely associated with multi-drug resistance. Moreover, overexpression of Hsp90 promoted β-catenin accumulation, while Hsp90 downregulation decreased the accumulation, nuclear translocation and transcriptional activity of β-catenin. We also identified that β-catenin was responsible for Hsp90-mediated expressions of P-gp, BCRP, Survivin, and Bcl-2. Furthermore, Hsp90 enhanced the AKT/GSK3β signaling, and AKT signaling played a critical role in Hsp90-induced accumulation and transcriptional activity of β-catenin, as well as multi-drug resistance to paclitaxel and cisplatin. In conclusion, Hsp90 enhanced the AKT/GSK3β/β-catenin signaling to induce multi-drug resistance of ovarian cancer. Suppressing Hsp90 chemosensitized multi-drug resistant ovarian cancer cells via impairing the AKT/GSK3β/β-catenin signaling, providing a promising therapeutic strategy for a successful treatment of ovarian cancer.

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