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Downregulation of VPS13C promotes cisplatin resistance in cervical cancer by upregulating GSTP1

ABSTRACT: Downregulation of VPS13C promotes cisplatin resistance in cervical cancer by upregulating GSTP1

PROVIDER: PRJNA985752 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24972219_1.fastq.gz	Fastqsanger.gz
	SRR24972219_2.fastq.gz	Fastqsanger.gz
	SRR24972220_1.fastq.gz	Fastqsanger.gz
	SRR24972220_2.fastq.gz	Fastqsanger.gz
	SRR24972221_1.fastq.gz	Fastqsanger.gz

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Downregulation of VPS13C promotes cisplatin resistance in cervical cancer by upregulating GSTP1 [SiHa]

Project description:Downregulation of VPS13C promotes cisplatin resistance in cervical cancer by upregulating GSTP1 [SiHa]

| PRJNA986107 | ENA

Downregulation of VPS13C promotes cisplatin resistance in cervical cancer by upregulating GSTP1

Project description:Cisplatin resistance remains a major obstacle limiting the effectiveness of chemotherapy in cervical cancer. However, the underlying mechanism of cisplatin resistance is still unclear.

2023-08-08 | GSE235366 | GEO

Downregulation of VPS13C promotes cisplatin resistance in cervical cancer by upregulating GSTP1 [SiHa]

2023-08-08 | GSE235466 | GEO

Combinatorial Treatment of Poly (ADP-ribose) Polymerase-1 Inhibitors and Cisplatin Attenuates Cervical Cancer Growth Through FOS-Driven Changes in Gene Expression

Project description:Cervical cancer is the one of the most prevalent types of cancers in women and is the second highest cause of death in women aged 20-39. The most common chemotherapy for cervical cancer involves the use of the drug cisplatin in conjunction with other therapeutics. However, the development of cisplatin resistance in patients can hinder the efficacy of these treatments. This highlights the need to explore different therapeutic approaches for cervical cancer treatment. We found that inhibitors targeting the enzyme Poly (ADP-ribose) Polymearse (PARP)-1 can attenuate cell growth of cervical adenocarcinoma and squamous cell carcinoma. Furthermore, combinatorial therapy of PARP inhibitors (PARPi) with cisplatin increases the cisplatin-mediated cell toxicity in cervical cancer cells. This is accompanied by a rewiring of the transcriptome in response to the cisplatin and PARPi together. Surprisingly, we observed that the Fos gene is upregulated in the dual treatment condition leading to the subsequent induction of its target genes. Importantly, increased the expression of Fos is sufficient to hinder cervical cancer growth. We conclude that by inducing Fos expression, PARPi treatment with cisplatin leads to inhibition of cervical cancer.

2022-08-02 | GSE176326 | GEO

KRT14 knockdown enhances cisplatin-resistance through upregulating LRP11 expression in ovarian cancer

Project description:KRT14 knockdown enhances cisplatin-resistance through upregulating LRP11 expression in ovarian cancer

| PRJNA1155994 | ENA

Upregulation of MMP3 promotes cisplatin resistance in ovarian cancer

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.

2025-04-24 | GSE275051 | GEO

CLPTM1L is a putative regulator of tumorigenesis and chemotherapy sensitization in cervical cancer

Project description:Cervical cancer stands as one of the leading causes of cancer-related mortality in women worldwide, yet the precise functions of host genes implicated in its pathogenesis remain elusive. Genome-wide association studies (GWAS) have revealed a significant association between the CLPTM1L locus and cervical cancer risk in European women, and aberrant expression of CLPTM1L has been noted in various malignant tumors. However, the role of CLPTM1L in cervical cancer remains largely unexplored. This study aimed to explore the biological function of CLPTM1L in cervical cancer. The expression of CLPTM1L in cervical cancer cells and tissues was detected by RT-qPCR. Furthermore, the potential biological functions of CLPTM1L in the context of cervical cancer were explored via RNA sequencing. Cell proliferation rates and the responsiveness of cervical cancer cells to cisplatin were evaluated using the CCK-8 assay, while cell apoptosis was quantified through the utilization of flow cytometry. Nude mouse xenograft models were utilized to explore the impact of CLPTM1L on tumor formation in vivo. Our findings demonstrated a significant increase in CLPTM1L mRNA expression levels in HeLa and C33A cells, as well as in cervical carcinoma tissues, compared to ECT1/E6E7 cells and adjacent normal tissues. Genes related to CLPTM1L were found to be enriched in the Hedgehog signaling pathway. In vitro and in vivo studies showed that reducing CLPTM1L expression markedly inhibited cell proliferation via downstream candidate genes BOC and LRP2. Furthermore, the downregulation of CLPTM1L was found to enhance cisplatin-induced cell apoptosis and increase the susceptibility of cervical cancer cells to cisplatin through DAP1. This investigation has bestowed upon us novel insights into the pathogenesis of cervical cancer, underscoring the potential of CLPTM1L as a promising target for chemotherapeutic sensitization in the management of this malignancy.

2024-08-31 | GSE267713 | GEO

Gene Expression in Cisplatin Resistance HeLa Cells

Project description:Cisplatin resistance is a problem in cancer treatment. Using DNA microarray, we detected differentially expressed genes in cisplatin-resistant cervix carcinoma HeLa cells compared to parental cells. Three cisplatin resistant cell lines were established by stepwise increasing cisplatin concentration. RNA from these resistant lines and its parental HeLa cells were labeled with Cy5 and Cy3. Equal amount of RNA from resistant cell line and HeLa were mixed and were hybridized to cDNA array. Signals were scanned and analyzed to find out the candidate genes involved in cisplatin resistant mechanism.

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KRT14 knockdown enhances cisplatin-resistance through upregulating LRP11 expression in ovarian cancer

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.

2025-04-17 | GSE276216 | GEO

Cancer-associated fibroblast-derived CCL5 promotes cisplatin resistance in neuroendocrine prostate cancer

Project description:Chemoresistance remains a significant challenge in the treatment of neuroendocrine prostate cancer (NEPC), a highly aggressive and lethal subtype of prostate cancer. Here, we identify a tumor-stromal interaction mediated by the CCL5/CCR5 signaling axis that drives cisplatin resistance. Cisplatin-induced DNA damage promotes a cGAS-STING–dependent senescence program in cancer-associated fibroblasts (CAFs), resulting in the secretion of CCL5, a key senescence-associated secretory phenotype factor. CAF-derived CCL5 binds to CCR5 on tumor cells, promoting the formation of a CCR5/β-arrestin1/p85 complex that activates the PI3K/AKT signaling pathway. This activation enhances DNA repair, protecting tumor cells from cisplatin-induced apoptosis. Pharmacologic inhibition of the CCL5/CCR5 pathway using maraviroc, an FDA-approved CCR5 antagonist, sensitizes NEPC cells to cisplatin treatment and significantly prolongs survival in an NEPC mouse model. These findings establish the CCL5/CCR5 axis as a critical mediator of tumor-stromal crosstalk and provide a promising therapeutic strategy for overcoming chemoresistance in NEPC.

2025-12-03 | GSE287963 | GEO

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