KRT14 knockdown enhances cisplatin-resistance through upregulating LRP11 expression in ovarian cancer
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1155994 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30521445_1.fastq.gz | Fastqsanger.gz | |||
| SRR30521445_2.fastq.gz | Fastqsanger.gz | |||
| SRR30521446_1.fastq.gz | Fastqsanger.gz | |||
| SRR30521446_2.fastq.gz | Fastqsanger.gz | |||
| SRR30521447_1.fastq.gz | Fastqsanger.gz |
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Project description:Ovarian cancer is a highly malignant gynecological tumor. Multidrug resistance (MDR) in tumors is a major reason for chemotherapy failure. Keratin 14 (KRT14), a member of the keratin family, plays a significant role across various cancers. Elevated KRT14 expression has been observed in ovarian cancer tissues compared to normal ovarian tissues, and this differential expression is associated with poorer progression-free survival in patients undergoing platinum and taxol-based chemotherapy. Furthermore, KRT14 expression is heightened in migratory ovarian cancer cells, where it plays a crucial role at the invasive interface, facilitating ovarian cancer cell invasion. The role of KRT14 in regulating MDR is not known. In this study, we aimed to investigate the effects and mechanisms of KRT14 in human cisplatin-resistant ovarian cancer cell lines SK-OV-3/DDP and A2780/DDP.
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Project description:Seventy percent of women with ovarian cancer develop resistance to cisplatin, contributing to persistently high mortality rates. Understanding the mechanisms behind this resistance is crucial for developing improved therapies. Matrix metalloproteinase 3 (MMP3) is elevated in ovarian cancer patients, but its role in cisplatin resistance remains underexplored. We observed significantly higher MMP3 protein and mRNA levels in cisplatin-resistant high-grade serous ovarian cancer (HGSOC) cells compared to cisplatin-sensitive cells, with further increases following cisplatin treatment. Kaplan‒Meier analysis indicated that patients with lower MMP3 levels have better survival outcomes. MMP3 knockdown via siRNA reduced cell viability, proliferation, and invasion, effects enhanced by cisplatin; however, a chemical MMP3 inhibitor did not replicate these effects. To better understand MMP3’s role, we conducted RNA sequencing to analyze gene expression changes and used immunoprecipitation with mass spectrometry to identify MMP3-interacting proteins, making this the first study to explore this in cisplatin-resistant ovarian cancer. Surprisingly, multiple injections of liposomal MMP3-siRNA increased tumor size in a mouse model, while combining MMP3-siRNA with cisplatin reduced tumor growth. These findings highlight MMP3’s complex role in cisplatin resistance and raise concerns about its targeting in vivo.
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Project description:Analysis of differences in DNA methylation in cisplatin-sensitive and cisplatin-resistant ovarian cancer cell lines.
2008-01-11 | E-TABM-210 | biostudies-arrayexpress
Project description:Platinum resistance is a major drawback in the treatment of ovarian cancer. Evidence suggests that microRNAs are key players in the initiation, progression, and drug resistance of cancer cells. However, the precise miRNAs dysregulated and contributing to platinum resistance in ovarian cancer cells have not been fully elucidated. Here, we conducted a miRNA expression profiling of cisplatin-sensitive (A2780) and cisplatin-resistant (CP20 and CIS) ovarian cancer cells to identify potential miRNAs involved in platinum resistance.
2020-11-20 | GSE161784 | GEO
Project description:Ovarian cancer (OC) is the most lethal gynecological tumor, primarily due to resistance to chemotherapy. Cyclin L2 (CCNL2), a novel member of the cyclin family, plays an important role in HIV replication. However, its role in OC chemoresistance remains unknown. Here, we demonstrate that elevated expression of CCNL2 indicates a poor prognosis in ovarian cancer. Furthermore, inhibition of CCNL2 reduces malignancy and enhances chemotherapy sensitivity in OC. Additionally, CCNL2 inhibition promotes cisplatin-induced ferroptosis by increasing intracellular iron ion levels. Mechanistically, CCNL2 is upregulated by YBX1 via a 5-methylcytosine (m5C) manner, leading to increased CCNL2 mRNA stability. Given the lack of protein structure data for CCNL2, we performed virtual screening to identify YBX1 inhibitors, targeting its upstream regulation. The inhibitor YB-B1 effectively suppresses YBX1 and CCNL2 expression, and enhances the cytotoxic effect of cisplatin. Together, we highlight the critical role of CCNL2 in ovarian cancer chemoresistance, elucidate its regulatory mechanism, and propose a new approach to address the challenge.
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Project description:Collagen type XI alpha 1 (COL11A1) is a novel biomarker associated with cisplatin resistance in ovarian cancer. However, the mechanisms underlying how COL11A1 confers cisplatin resistance in ovarian cancer are poorly understood. We identified that fatty acid β-oxidation (FAO) is upregulated by COL11A1 in ovarian cancer cells and that COL11A1-driven cisplatin resistance can be abrogated by inhibition of FAO. Furthermore, our results demonstrate that COL11A1 also enhances the expression of proteins involved in fatty acid synthesis. Interestingly, COL11A1-induced upregulation of fatty acid synthesis and FAO is modulated by the same signaling molecules. We identified that binding of COL11A1 to its receptors, α1β1 integrin and discoidin domain receptor 2 (DDR2), activates Src-Akt-AMPK signaling to increase the expression of both fatty acid synthesis and oxidation enzymes, although DDR2 seems to be the predominant receptor. Inhibition of fatty acid synthesis downregulates FAO despite the presence of COL11A1, suggesting that fatty acid synthesis might be a driver of FAO in ovarian cancer cells. Taken together, our results suggest that COL11A1 upregulates fatty acid metabolism in ovarian cancer cells in a DDR2-Src-Akt-AMPK dependent manner. Therefore, we propose that blocking FAO might serve as a promising therapeutic target to treat ovarian cancer, particularly cisplatin-resistant recurrent ovarian cancers which typically express high levels of COL11A1.
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Project description:To determine the signaling networks that are dysregulated in platinum-resistant ovarian cancer, gene expression data were obtained from, and compared between, the ovarian cancer cell line, A2780, and its cisplatin-resistant derivative, A2780cis. Gene expression data from a cisplatin-sensitive ovarian cancer cell line (A2780) were collected and compared to gene expression data from a cisplatin-resistant cell line (A2780cis). 6 independent experiments were completed for both the sensitive and resistant cell lines.
2011-11-05 | E-GEOD-33482 | biostudies-arrayexpress
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.
2016-07-06 | PXD001176 | Pride
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Project description:Chemo-resistance to platinum such as cisplatin is critical in the treatment of ovarian cancer. Recent evidences have linked epithelial-mesenchymal transition (EMT) with the drug resistance as a contributing mechanism. The current study explored the connection between cellular responses to cisplatin with EMT in ovarian cancer. 46 ovarian carcinoma cell lines expression data with and without Cisplatin treatment.
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