scholarly journals Deregulation of IKBKE Is Associated with Tumor Progression, Poor Prognosis, and Cisplatin Resistance in Ovarian Cancer

2009 ◽  
Vol 175 (1) ◽  
pp. 324-333 ◽  
Author(s):  
Jian-Ping Guo ◽  
Shao-Kun Shu ◽  
Lili He ◽  
Yi-Chun Lee ◽  
Patricia A. Kruk ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Tumor Progression ◽  
Poor Prognosis ◽  
Cisplatin Resistance

scholarly journals OTUB1-catalyzed deubiquitination of FOXM1 facilitates tumor progression and predicts a poor prognosis in ovarian cancer

Oncotarget ◽  
2016 ◽  
Vol 7 (24) ◽  
pp. 36681-36697 ◽  
Author(s):  
Yiqin Wang ◽  
Xianrong Zhou ◽  
Midie Xu ◽  
Weiwei Weng ◽  
Qiongyan Zhang ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Tumor Progression ◽  
Poor Prognosis

scholarly journals Expression of stress-induced phosphoprotein1 (STIP1) is associated with tumor progression and poor prognosis in epithelial ovarian cancer

2014 ◽  
Vol 53 (4) ◽  
pp. 277-288 ◽  
Author(s):  
Hanbyoul Cho ◽  
Sunghoon Kim ◽  
Ha-Yeon Shin ◽  
Eun Joo Chung ◽  
Haruhisa Kitano ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Epithelial Ovarian Cancer ◽  
Tumor Progression ◽  
Poor Prognosis

Upregulation of microRNA-203 is associated with advanced tumor progression and poor prognosis in epithelial ovarian cancer

2013 ◽  
Vol 30 (3) ◽  
Author(s):  
Shaosheng Wang ◽  
Xiaohong Zhao ◽  
Jie Wang ◽  
Yingmei Wen ◽  
LinJing Zhang ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Epithelial Ovarian Cancer ◽  
Tumor Progression ◽  
Poor Prognosis ◽  
Advanced Tumor

scholarly journals Targeting ACLY Attenuates Tumor Growth and Acquired Cisplatin Resistance in Ovarian Cancer by Inhibiting PI3K/AKT Pathway and Activating AMPK/ROS Pathway

2020 ◽  
Author(s):  
Xuan Wei ◽  
Juanjuan Shi ◽  
Qianhan Lin ◽  
Xiaoxue Ma ◽  
Yingxin Pang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Mtt Assay ◽  
Poor Prognosis ◽  
Cisplatin Resistance ◽  
Bioinformatic Analysis ◽  
Akt Pathway ◽  
Cancer Tissue ◽  
Elevated Concentration

Abstract Background: Ovarian cancer is the most lethal female genital malignancy. Though cisplatin is still the first-line chemotherapy to treat ovarian cancer patients with debulking surgeries, its efficacy is limited due to the high-incidence of cisplatin resistance. ATP citrate lyase (ACLY) has been proved to be a key metabolic enzyme and was related to poor prognosis in various cancer, including ovarian cancer. Nevertheless, there has not been any research elucidating the relationship between ACLY and cisplatin resistance and the mechanism of how it works.Methods: Survival analysis was mainly carried out on the website. Bioinformatic analysis was performed in R/R studio. Proliferative activity was measured by MTT assay and colony formation assay. Cell cycle and apoptosis analysis were performed by flow cytometry. Acquired cisplatin resistant cell line A2780/CDDP was generated from A2780 by exposing to gradually elevated concentration of cisplatin. MTT assay was used to calculate IC50 of cisplatin. Xenograft tumor assay was used test cell proliferation in vivo.Results: Higher expression of ACLY was found in ovarian cancer tissue and related to poor prognosis. Knockdown of ACLY in A2780, SKOV3 and HEY cells inhibited cell proliferation, caused cell cycle arrest by modulating P16/CDK4/CCDN1 pathway and induced apoptosis probably by inhibiting p-AKT activity. Bioinformatic analysis of GSE15709 dataset revealed upregulation of ACLY and activation of PI3K/AKT pathway in acquired cisplatin resistant cells, in line with the results of A2780/CDDP cells generated by us. Knockdown of ACLY could alleviate cisplatin resistance and work synergistically with cisplatin treatment in inducing apoptosis in A2780/CDDP cells, by inhibiting PI3K/AKT pathway and activating AMPK/ROS pathway. ACLY specific inhibitor SB-204990 also showed the same effect. In A2780/CDDP cells, AKT overexpression could destroy cisplatin re-sensitization caused by ACLY knockdown. Conclusions: Knockdown of ACLY attenuated cisplatin resistance by inhibiting PI3K/AKT pathway and activating AMPK/ROS pathway. These findings suggested that combination of ACLY inhibition and cisplatin could be an effective strategy for overcoming cisplatin resistance in ovarian cancer.

scholarly journals Targeting ACLY Attenuates Tumor Growth and Acquired Cisplatin Resistance in Ovarian Cancer by Inhibiting the PI3K–AKT Pathway and Activating the AMPK–ROS Pathway

2021 ◽  
Vol 11 ◽  
Author(s):  
Xuan Wei ◽  
Juanjuan Shi ◽  
Qianhan Lin ◽  
Xiaoxue Ma ◽  
Yingxin Pang ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Poor Prognosis ◽  
Cisplatin Resistance ◽  
Specific Inhibitor ◽  
Bioinformatic Analysis ◽  
Akt Pathway ◽  
Metabolic Enzyme ◽  
Cancer Tissue

Background: Ovarian cancer is the most lethal female genital malignancy. Although cisplatin is the first-line chemotherapy to treat ovarian cancer patients along with debulking surgeries, its efficacy is limited due to the high incidence of cisplatin resistance. ATP citrate lyase (ACLY) has been shown to be a key metabolic enzyme and is associated with poor prognosis in various cancers, including ovarian cancer. Nevertheless, no studies have probed the mechanistic relationship between ACLY and cisplatin resistance.Methods: Survival analysis was mainly carried out online. Bioinformatic analysis was performed in R/R studio. Proliferative activity was measured by MTT and colony formation assays. Cell cycle and apoptosis analysis were performed by flow cytometry. The acquired-cisplatin-resistant cell line A2780/CDDP was generated by exposing A2780 to cisplatin at gradually elevated concentrations. MTT assay was used to calculate IC50 values of cisplatin. A xenograft tumor assay was used test cell proliferation in vivo.Results: Higher expression of ACLY was found in ovarian cancer tissue and related to poor prognosis. Knockdown of ACLY in A2780, SKOV3, and HEY cells inhibited cell proliferation, caused cell-cycle arrest by modulating the P16–CDK4–CCND1 pathway, and induced apoptosis probably by inhibiting p-AKT activity. Bioinformatic analysis of the GSE15709 dataset revealed upregulation of ACLY and activation of PI3K–AKT pathway in cells with acquired cisplatin resistance, in line with observations on A2780/CDDP cells that we generated. Knockdown of ACLY alleviated cisplatin resistance, and works synergistically with cisplatin treatment to induce apoptosis in A2780/CDDP cells by inhibiting the PI3K–AKT pathway and activating AMPK–ROS pathway. The ACLY-specific inhibitor SB-204990 showed the same effect. In A2780/CDDP cells, AKT overexpression could attenuate cisplatin re-sensitization caused by ACLY knockdown.Conclusions: Knockdown of ACLY attenuated cisplatin resistance by inhibiting the PI3K–AKT pathway and activating the AMPK–ROS pathway. These findings suggest that a combination of ACLY inhibition and cisplatin might be an effective strategy for overcoming cisplatin resistance in ovarian cancer.

Expression of 67-kDa laminin receptor was associated with tumor progression and poor prognosis in epithelial ovarian cancer

2012 ◽  
Vol 125 (2) ◽  
pp. 427-432 ◽  
Author(s):  
Taejong Song ◽  
Chel Hun Choi ◽  
Young Jae Cho ◽  
Chang Ohk Sung ◽  
Sang Yong Song ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Epithelial Ovarian Cancer ◽  
Tumor Progression ◽  
Poor Prognosis ◽  
Laminin Receptor

PRSS3 expression is associated with tumor progression and poor prognosis in epithelial ovarian cancer

2015 ◽  
Vol 137 (3) ◽  
pp. 546-552 ◽  
Author(s):  
Ruiqiong Ma ◽  
Xue Ye ◽  
Hongyan Cheng ◽  
Yu Ma ◽  
Heng Cui ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Epithelial Ovarian Cancer ◽  
Tumor Progression ◽  
Poor Prognosis
Sign in / Sign up

Export Citation Format

Share Document