Dataset Information

Ovarian cancer cell line LC-MS-MS

ABSTRACT: A2780-DR cells are cisplatin resistance compared to A2780. H19 knockdown in A2780-DR cells resulted in recovery of cisplatin sensitivity in vitro and in vivo. To demonstrate how H19 contributes to cisplatin-resistance in ovarian cancer, proteomic analysis was carried out on A2780, A2780-DR, A2780-DR/H19si, and A2780-DR/control cells. Proteins expression levels were identified and quantified using MaxQuant software (http://medusa.biochem.mpg.de/maxquant_doku/). The experiments were repeated twice and the false-positive rate was set to be <1%. Based on label-free quantification intensity ratios (>1.67 or <0.6) in proteins that have two or more unique peptides.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture, Cell Line Cell

DISEASE(S): Malignant Neoplasm Of Ovary

SUBMITTER: Hong Xu

LAB HEAD: Yue-Jin Hua

PROVIDER: PXD003252 | Pride | 2018-10-25

REPOSITORIES: Pride

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Publications

The Essential Role of H19 Contributing to Cisplatin Resistance by Regulating Glutathione Metabolism in High-Grade Serous Ovarian Cancer.

Zheng Zhi-Guo ZG Xu Hong H Suo Sha-Sha SS Xu Xiao-Li XL Ni Mao-Wei MW Gu Lin-Hui LH Chen Wei W Wang Liang-Yan LY Zhao Ye Y Tian Bing B Hua Yue-Jin YJ

Scientific reports 20160519

Primary and acquired drug resistance is one of the main obstacles encountered in high-grade serous ovarian cancer (HGSC) chemotherapy. Cisplatin induces DNA damage through cross-linking and long integrated non-coding RNAs (lincRNAs) play an important role in chemical induced DNA-damage response, which suggests that lincRNAs may be also associated with cisplatin resistance. However, the mechanism of long integrated non-coding RNAs (lincRNAs) acting on cisplatin resistance is not well understood. ...[more]

PMID: 27193186

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Project description:Drug resistance poses a major challenge to ovarian cancer treatment. Understanding mechanisms of drug resistance is important for finding new therapeutic targets. In the present work, a cisplatin-resistant ovarian cancer cell line A2780-DR was established with a resistance index of 6.64. The cellular accumulation of cisplatin was significantly reduced in A2780-DR cells as compared to A2780 cells consistent with the general character of drug resistance. Quantitative proteomic analysis identified 340 differentially expressed proteins between A2780 and A2780-DR cells, which involve in diverse cellular processes, including metabolic process, cellular component biogenesis, cellular processes and stress responses. Expression levels of Ras-related proteins Rab 5C and Rab 11B in A2780-DR cells were lower than those in A2780 cells as confirmed by real-time quantitative PCR and western blotting. The short hairpin (sh)RNA-mediated knockdown of Rab 5C in A2780 cells resulted in markedly increased resistance to cisplatin whereas overexpression of Rab 5C in A2780-DR cells increases sensitivity to cisplatin, demonstrating that Rab 5C-dependent endocytosis plays an important role in cisplatin resistance. Our results also showed that expressions of glycolytic enzymes PKM, GPI, Aldolase, LDH, and PGK were down-regulated in drug resistant cells, indicating drug resistance in ovarian cancer is directly associated with a decrease in glycolysis. Furthermore, it was found that glutathione reductase were up-regulated in A2780-DR, while vimentin, HSP90, and Annexin A1 and A2 were down-regulated. Taken together, our results suggest that drug resistance in ovarian cancer cell line A2780 is caused by multifactorial traits, including the down-regulation of Rab 5C-dependent endocytosis of cisplatin, glycolytic enzymes and vimentin, and up-regulation of antioxidant proteins, suggesting Rab 5C is a potential target for treatment of drug-resistant ovarian cancer. This constitutes a further step towards a comprehensive understanding of drug resistance in ovarian cancer.

			Action	DRS
	A2780-1.msf	Msf
	A2780-1.raw	Raw
	A2780-2.raw	Raw
	A2780-DR-1.msf	Msf
	A2780-DR-1.raw	Raw