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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

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.

2010-05-06 | E-GEOD-15120 | biostudies-arrayexpress

CMTM6 drives cisplatin resistance by regulating AKT mediated Wnt signaling

Project description:The RNA-seq library preparation was performed for H357 CisR Nt Sh and H357 CisR CMTM6 shRNA treated with vehicle control (UT) and cisplatin (10 μM) (CisT) for 24 h. We have included two independent biological replicates to identify the CMTM6 downregulation mediated global transcriptome changes. For RNA-seq library preparation 2 μg of total RNA was used to isolate mRNA through magnetic beads using mRNA isolation kit (PolyA mRNA isolation Module, NEB) followed by RNA-seq library preparation using mRNA library preparation kit (NEB) strictly following the vendor recommended protocol. After library preparation concentration of libraries was estimated using qubit 2.0 (Invitrogen) and the recommended fragmentation sizes were confirmed by Tapestation (Agilent).

2021-02-08 | E-MTAB-9424 | biostudies-arrayexpress

Gene expression data from parental HeLa and Dickkopf-1 (Dkk1) knockout HeLa cells after Cisplatin treatment

Project description:Infection with oncogenic human papillomavirus (HPV) is a major cause for the development of cervical cancer, which is mainly driven by the expression of the HPV E6 and E7 oncoproteins. We uncovered that the concentration levels of the putative tumor suppressor Dickkopf-1 (Dkk1) are restricted in cervical cancer cells by HPV E6 expression due to the E6-mediated proteolytic degradation of p53, which is a transcriptional regulator of Dkk1. Moreover, we found that Dkk1 is critically involved in the pro-apoptotic Cisplatin response of these cells, as Dkk1 repression was associated with an increased resistance towards the chemotherapeutic compound. This could be of high relevance for cervical cancer treatments, which usually involve Cisplatin for standard care. Although Dkk1 is a major antagonist of the canonical Wnt signaling, the differential response towards Cisplatin observed in Dkk1-depleted cells was not associated to an activation of this pathway. To elucidate alternative underlying mechanisms, we performed Affymetrix Gene Expression analyses comparing the transcriptome of Cisplatin-treated parental HeLa to CRISPR/Cas9-generated Dkk1 knockout (KO) HeLa cells. These revealed that Dkk1 depletion is linked to an impairment of the pro-apoptotic JNK/AP-1 pathway in cervical cancer cells, suggesting that Dkk1 drives Cisplatin-mediated apoptosis via activation of this signaling hub.

2022-08-16 | GSE200748 | GEO

Gene Expression in Cisplatin Resistance HeLa Cells

2010-03-05 | GSE15120 | GEO

The non-apoptotic function of Caspase-8 in negatively regulating the CDK9 mediated Ser2 phosphorylation of RNA Polymerase II in cervical cancer

Project description:Cervical cancer is the fourth most frequently diagnosed and fatal gynecological cancer. 15-61% of all cases metastasize and develop chemoresistance, reducing the 5-year survival of cervical cancer patients to as low as 17%. Therefore, unraveling the mechanisms contributing to metastasis is critical in developing better-targeted therapies against it. Here, we have identified a novel mechanism where nuclear Caspase-8 directly interacts with and inhibits the activity of CDK9, thereby modulating RNAPII-mediated global transcription, including those of cell-migration and -invasion-associated genes. Crucially, low Caspase-8 expression in cervical cancer patients leads to poor prognosis, higher CDK9 phosphorylation at Thr186, and increased RNAPII activity in cervical cancer cell lines and patient biopsies. Caspase-NT8 knock-out cells were also more resistant to the small-molecule CDK9 inhibitor BAY1251152 in both 2D- and 3D-culture conditions. Combining BAY1251152 with Cisplatin synergistically overcame chemoresistance of Caspase-8 deficient cervical cancer cells. Therefore, Caspase-8 expression could be a marker in chemoresistant cervical tumors, suggesting CDK9 inhibitor treatment for their sensitization to Cisplatin-based chemotherapy.

2023-03-11 | PXD038102 | Pride

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