Resistance to chemotherapy-induced apoptosis via decreased caspase-3 activity and overexpression of antiapoptotic proteins in ovarian cancer

Xiaokui Yang; Fang Zheng; Hui Xing; Qinglei Gao; Wang Wei; Yunping Lu; Shixuan Wang; Jianfeng Zhou; Wei Hu; Ding Ma

doi:10.1007/s00432-004-0556-9

Resistance to chemotherapy-induced apoptosis via decreased caspase-3 activity and overexpression of antiapoptotic proteins in ovarian cancer

Xiaokui Yang, Fang Zheng, Hui Xing, Qinglei Gao, Wang Wei, Yunping Lu, Shixuan Wang, Jianfeng Zhou, Wei Hu, Ding Ma

Gynecological Oncology & Reproductive Medicine

Research output: Contribution to journal › Article › peer-review

86 Scopus citations

Abstract

Goals: Resistance to cisplatin is the main reason for treatment failure in ovarian cancer. Apoptosis is the main mechanism of action of most cancer chemotherapeutic agents. The apoptosis-associated proteins expressed in cisplatin-sensitive (A2780, COC1) and -resistant (A2780/DDP, COC1/DDP) ovarian cancer cell lines, as well as their effects on caspase-3 activity in these cells, were studied by reverse transcriptase polymerase chain reaction and Western blot analysis. Methods: The apoptotic ratios of A2780, COC1, A2780/DDP, and COC1/DDP cells after treatment with cisplatin were measured by flow cytometry. Results: Expression of Bcl-2 and Bcl-X_L in A2780/DDP and COC1/DDP cells was significantly higher than that in A2780 and COC1 cells, respectively. Expression of Bax and Bcl-Xs did not differ in cisplatin-resistant and -sensitive cells. Caspase-3 activity was reduced markedly and apoptotic ratios were significantly lower in A2780/DDP and COC1/DDP cells than in A2780 and COC1 cells after treatment with cisplatin. Conclusion: We conclude that overexpression of antiapoptotic proteins Bcl-2 and Bcl-X_L and down-regulation of caspase-3 activity may be associated with cisplatin resistance in human ovarian cancer.

Original language	English (US)
Pages (from-to)	423-428
Number of pages	6
Journal	Journal of cancer research and clinical oncology
Volume	130
Issue number	7
DOIs	https://doi.org/10.1007/s00432-004-0556-9
State	Published - Jul 2004

Keywords

Apoptosis
Bcl-2
Caspase-3
Chemoresistance
Cisplatin (cis-diamine-dichloro-platinum)
Ovarian neoplasm

ASJC Scopus subject areas

Oncology
Cancer Research

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10.1007/s00432-004-0556-9

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@article{2a29dfd2c2004d84ba10dae3e8ed88bc,

title = "Resistance to chemotherapy-induced apoptosis via decreased caspase-3 activity and overexpression of antiapoptotic proteins in ovarian cancer",

abstract = "Goals: Resistance to cisplatin is the main reason for treatment failure in ovarian cancer. Apoptosis is the main mechanism of action of most cancer chemotherapeutic agents. The apoptosis-associated proteins expressed in cisplatin-sensitive (A2780, COC1) and -resistant (A2780/DDP, COC1/DDP) ovarian cancer cell lines, as well as their effects on caspase-3 activity in these cells, were studied by reverse transcriptase polymerase chain reaction and Western blot analysis. Methods: The apoptotic ratios of A2780, COC1, A2780/DDP, and COC1/DDP cells after treatment with cisplatin were measured by flow cytometry. Results: Expression of Bcl-2 and Bcl-XL in A2780/DDP and COC1/DDP cells was significantly higher than that in A2780 and COC1 cells, respectively. Expression of Bax and Bcl-Xs did not differ in cisplatin-resistant and -sensitive cells. Caspase-3 activity was reduced markedly and apoptotic ratios were significantly lower in A2780/DDP and COC1/DDP cells than in A2780 and COC1 cells after treatment with cisplatin. Conclusion: We conclude that overexpression of antiapoptotic proteins Bcl-2 and Bcl-XL and down-regulation of caspase-3 activity may be associated with cisplatin resistance in human ovarian cancer.",

keywords = "Apoptosis, Bcl-2, Caspase-3, Chemoresistance, Cisplatin (cis-diamine-dichloro-platinum), Ovarian neoplasm",

author = "Xiaokui Yang and Fang Zheng and Hui Xing and Qinglei Gao and Wang Wei and Yunping Lu and Shixuan Wang and Jianfeng Zhou and Wei Hu and Ding Ma",

note = "Funding Information: Acknowledgement The authors are grateful to Fily Gao for technical support. This work was supported by grants from the National Science Foundation of China (No. 30025017) and {\textquoteleft}{\textquoteleft}973{\textquoteright}{\textquoteright} Program of China (No. 2002CB513107).",

year = "2004",

month = jul,

doi = "10.1007/s00432-004-0556-9",

language = "English (US)",

volume = "130",

pages = "423--428",

journal = "Journal of cancer research and clinical oncology",

issn = "0171-5216",

publisher = "Springer Verlag",

number = "7",

}

TY - JOUR

T1 - Resistance to chemotherapy-induced apoptosis via decreased caspase-3 activity and overexpression of antiapoptotic proteins in ovarian cancer

AU - Yang, Xiaokui

AU - Zheng, Fang

AU - Xing, Hui

AU - Gao, Qinglei

AU - Wei, Wang

AU - Lu, Yunping

AU - Wang, Shixuan

AU - Zhou, Jianfeng

AU - Hu, Wei

AU - Ma, Ding

N1 - Funding Information: Acknowledgement The authors are grateful to Fily Gao for technical support. This work was supported by grants from the National Science Foundation of China (No. 30025017) and ‘‘973’’ Program of China (No. 2002CB513107).

PY - 2004/7

Y1 - 2004/7

N2 - Goals: Resistance to cisplatin is the main reason for treatment failure in ovarian cancer. Apoptosis is the main mechanism of action of most cancer chemotherapeutic agents. The apoptosis-associated proteins expressed in cisplatin-sensitive (A2780, COC1) and -resistant (A2780/DDP, COC1/DDP) ovarian cancer cell lines, as well as their effects on caspase-3 activity in these cells, were studied by reverse transcriptase polymerase chain reaction and Western blot analysis. Methods: The apoptotic ratios of A2780, COC1, A2780/DDP, and COC1/DDP cells after treatment with cisplatin were measured by flow cytometry. Results: Expression of Bcl-2 and Bcl-XL in A2780/DDP and COC1/DDP cells was significantly higher than that in A2780 and COC1 cells, respectively. Expression of Bax and Bcl-Xs did not differ in cisplatin-resistant and -sensitive cells. Caspase-3 activity was reduced markedly and apoptotic ratios were significantly lower in A2780/DDP and COC1/DDP cells than in A2780 and COC1 cells after treatment with cisplatin. Conclusion: We conclude that overexpression of antiapoptotic proteins Bcl-2 and Bcl-XL and down-regulation of caspase-3 activity may be associated with cisplatin resistance in human ovarian cancer.

AB - Goals: Resistance to cisplatin is the main reason for treatment failure in ovarian cancer. Apoptosis is the main mechanism of action of most cancer chemotherapeutic agents. The apoptosis-associated proteins expressed in cisplatin-sensitive (A2780, COC1) and -resistant (A2780/DDP, COC1/DDP) ovarian cancer cell lines, as well as their effects on caspase-3 activity in these cells, were studied by reverse transcriptase polymerase chain reaction and Western blot analysis. Methods: The apoptotic ratios of A2780, COC1, A2780/DDP, and COC1/DDP cells after treatment with cisplatin were measured by flow cytometry. Results: Expression of Bcl-2 and Bcl-XL in A2780/DDP and COC1/DDP cells was significantly higher than that in A2780 and COC1 cells, respectively. Expression of Bax and Bcl-Xs did not differ in cisplatin-resistant and -sensitive cells. Caspase-3 activity was reduced markedly and apoptotic ratios were significantly lower in A2780/DDP and COC1/DDP cells than in A2780 and COC1 cells after treatment with cisplatin. Conclusion: We conclude that overexpression of antiapoptotic proteins Bcl-2 and Bcl-XL and down-regulation of caspase-3 activity may be associated with cisplatin resistance in human ovarian cancer.

KW - Apoptosis

KW - Bcl-2

KW - Caspase-3

KW - Chemoresistance

KW - Cisplatin (cis-diamine-dichloro-platinum)

KW - Ovarian neoplasm

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U2 - 10.1007/s00432-004-0556-9

DO - 10.1007/s00432-004-0556-9

M3 - Article

C2 - 15156398

AN - SCOPUS:3843115557

SN - 0171-5216

VL - 130

SP - 423

EP - 428

JO - Journal of cancer research and clinical oncology

JF - Journal of cancer research and clinical oncology

IS - 7

ER -

Resistance to chemotherapy-induced apoptosis via decreased caspase-3 activity and overexpression of antiapoptotic proteins in ovarian cancer

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