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Regulation of the error-prone DNA polymerase polκ by oncogenic signaling and its contribution to drug resistance

ABSTRACT: We report how the A375 melanoma cell line changes following CRISPR-Cas9 inactivation of POLK

ORGANISM(S): Homo sapiens

PROVIDER: GSE145313 | GEO | 2020/02/15

REPOSITORIES: GEO

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Regulation of the error-prone DNA polymerase Polκ by oncogenic signaling and its contribution to drug resistance.

Project description: Not available

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Catestatin impedes melanoma progression and drug resistance by reprogramming oncogenic signaling pathways

Project description:Melanoma remains one of the most aggressive and treatment-resistant cancers, emphasizing the need for novel therapeutics. In our current study we report a peptide-based approach as potential therapeutic. The expression and role of Catestatin(CST), a Chromogranin A(CgA)-derived peptide with immunomodulatory and reparative properties in skin injury led us to examine its connection to melanoma. Advancing melanoma stages showed decreased CST expression. CST administration to patient derived cells and melanoma cell lines A375, B16F10, SKMEL28 revealed increased apoptosis, decreased proliferation and metastatic ability of the melanoma cells without affecting cell viability for normal skin fibroblasts. CST reduced growth kinetics and tumor weight in B16F10 derived in vivo melanoma tumors. Transcriptomic analyses of catestatin treated human cell line and mouse tumor revealed downregulation of hypoxia, collagen remodeling, epithelial to mesenchymal transition pathways (EMT), stress adaptive responses that are accountable for melanoma progression. In Vemurafenib-resistant A375 cells, CST increased apoptosis and repressed multiple resistance associated genes. These results highlight CST as a promising therapeutic candidate capable of opposing melanoma progression and overcoming resistance to current targeted treatments.

2026-03-16 | GSE312638 | GEO

Regulation of the error-prone DNA polymerase polκ by oncogenic signaling and its contribution to drug resistance

Project description:Regulation of the error-prone DNA polymerase polκ by oncogenic signaling and its contribution to drug resistance

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poliota, a remarkably error-prone human DNA polymerase.

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Cancer genes disfavoring T cell immunity identified via integrated systems approach

Project description:A375 melanoma cells were transduced with Cas9 and non-targeting (NT) or BIRC2-targeting sgRNAs. Cells were cultured for 20 days post gene-editing and cell pellets were collected for analysis. Separately, A375 melanoma cells were treated with LCL161 for 16 hours and cell pellets were collected for analysis.

2022-06-27 | MSV000089737 | MassIVE

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Project description: Not available

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The putative error prone polymerase <i>REV1</i> mediates DNA damage and drug resistance in <i>Candida albicans</i>.

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Comparative gene expression profiles of NOS1-KO and WT A375 melanoma cell lines

Project description:NOS1 plays a vital role in tumor. A cell model of NOS1 gene knockout in human melanoma cell line A375 was constructed using CRISPR/Cas9 technique for the study of its function. We used microarrays to detail the Global gene expression underlying NOS1-knockout compare to wild type A375 cell.

2021-12-31 | GSE166287 | GEO

A role for the putative error-prone polymerase REV1 in DNA damage and antifungal drug resistance in Candida albicans

Project description:Antimicrobial-induced DNA damage, and subsequent repair via upregulation of DNA repair factors, including error-prone translesion polymerases, can lead to the increased accumulation of mutations in the microbial genome, and ultimately increased risk of acquired mutations associated with antimicrobial resistance. While this phenotype is well described in bacterial species, it is less thoroughly investigated amongst microbial fungi. Here, we monitor DNA damage induced by antifungal agents in the fungal pathogen Candida albicans, and find that commonly used antifungal drugs are able to induce DNA damage, leading to the upregulation of transcripts encoding predicted error-prone polymerases and related factors. We focus on REV1, encoding a putative error-prone polymerase, and find that while deleting this gene in C. albicans leads to increased sensitivity to DNA damage, it also unexpectedly renders cells more likely to incur mutations and evolve resistance to antifungal agents. We further find that deletion of REV1 leads to a significant depletion in the uncharacterized protein Shm1, which itself plays a role in fungal mutagenesis. Together, this work lends new insight into previously uncharacterized factors with important roles in the DNA damage response, mutagenesis, and the evolution of antifungal drug resistance.

2025-05-07 | PXD055008 | Pride

INO80 governs super-enhancer-mediated oncogenic transcription and tumor growth in melanoma [ChIP-seq_MiSeq]

Project description:Super-enhancers (SEs) are large genomic regions with high density of enhancer marks. In cancer, SEs are found near oncogenes and dictate cancer gene expression. However, how oncogenic SEs are regulated remains poorly understood. Here, we show that INO80, a chromatin remodeling complex, is required for SE-mediated oncogenic transcription and tumor growth in melanoma. The expression of Ino80, the SWI/SNF ATPase, is elevated in melanoma cells and patient melanomas compared to normal melanocytes and benign nevi. Furthermore, Ino80 silencing selectively inhibits melanoma cell proliferation, anchorage-independent growth, as well as tumorigenesis and tumor maintenance in mouse xenografts. Mechanistically, Ino80 occupies more than 90% of SEs, and its occupancy is dependent on transcription factors such as MITF and Sox9. Ino80 binding reduces nucleosome occupancy and facilitates Mediator recruitment, thus promoting oncogenic transcription. Consistently, genes co-occupied by Ino80 and Med1 are specifically expressed in melanomas compared to melanocytes. Together, our results reveal an essential role of INO80-dependent chromatin remodeling in SE function, and suggest a novel strategy for disrupting SEs in cancer treatment. Human melanoma cell line A375 cells were infected with shNT or shIno80, and total RNA was extracted 2, 3, 4 days after infection. The RNA was submitted to RNA-Seq subsequently. For ChIP-Seq, either wild type A375 and SK-MEL-147, or A375 infected with shNT or shIno80, was used for ChIP-Seq for corresponding factors.

2016-07-07 | E-GEOD-82331 | biostudies-arrayexpress

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