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Polyploid cisplatin-resistant cancer cells have altered nuclear organization and epigenomic status

ABSTRACT: Polyploid cisplatin-resistant cancer cells have altered nuclear organization and epigenomic status

PROVIDER: PRJNA1271763 | ENA |

REPOSITORIES: ENA

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Polyploid cisplatin-resistant cancer cells have altered nuclear organization and epigenomic status

Project description:Chemotherapy resistance remains a critical barrier in cancer treatment, partly driven by polyploid cells that survive therapy and contribute to tumor recurrence. Here, we investigated epigenomic and transcriptional changes associated with cisplatin-surviving polyploid cells compared to parental cancer cells in prostate cancer (PC3) and triple-negative breast cancer (MDA-MB-231) cell lines. We observed persistent dysregulation of chromatin compaction and altered nuclear structure in polyploid cells following cisplatin treatment. Genome-wide chromatin accessibility profiling via ATAC-seq revealed significant remodeling, notably decreased promoter accessibility at proliferation-associated loci and increased accessibility of distal regulatory elements linked to inflammation and stress response. RNA-seq analyses demonstrated a coordinated transcriptional shift away from proliferative signatures toward inflammatory and survival pathways, including activation of NFκB, interferon response, and integrated stress response pathways. Importantly, we identified subsets of genes showing concordant changes in promoter accessibility and transcriptional activity, directly linking chromatin remodeling to transcriptional reprogramming. These integrated findings highlight the role of chromatin dynamics and epigenetic plasticity in chemotherapy resistance, demonstrating that widespread chromatin accessibility changes facilitate the transition to a stress-adapted, polyploid cell state. This study provides new insights into the molecular mechanisms supporting cancer cell persistence after chemotherapy.

2025-06-30 | GSE298905 | GEO

Polyploid cancer cells reveal signatures of chemotherapy relapse [scRNA-seq]

Project description:Treatment of PC3 and MDA-MB-231 cell lines with sublethal doses of docetaxel or cisplatin in vitro resulted in induction of polyploid cancer cells. Single cell copy RNA-sequencing was conducted to understand resistance of polyploid cancer cells to chemotherapy.

2024-09-13 | GSE270568 | GEO

Polyploid cancer cells reveal signatures of chemotherapy relapse [scDNA-seq]

Project description:Treatment of PC3 and MDA-MB-231 cell lines with sublethal doses of docetaxel or cisplatin in vitro resulted in induction of polyploid cancer cells. Single cell copy number profiling was conducted to understand resistance of polyploid cancer cells to chemotherapy.

2024-09-13 | GSE270567 | GEO

Gene expression changes during aging in polyploid and diploid hepatocytes

Project description:To examine gene expression changes duging aging in polyploid and diploid hepatocytes, diploid and polyploid hepatocytes were sorted from young and aged multi-reporter mice and their gene expressions were analyzed by high-throughput RNA sequence.

2021-04-14 | GSE161171 | GEO

Genes altered in expression by Cisplatin treatment in lung cancer cell lines

Project description:Genes altered by Cisplatin treatment and long term-cultured in lung cancer cell lines

2019-11-05 | GSE139887 | GEO

CDK2 Inhibition Produces a Persistent Population of Polyploid Cancer Cells

Project description:Aneuploidy, a cancer hallmark, drives chromosomal instability, drug resistance, and clinically-aggressive tumors. Cyclin-dependent kinase 2 (CDK2) antagonism with independent inhibitors or CDK2 knock-down triggered anaphase catastrophe. This disrupts supernumerary centrosome clustering, causing multipolar division and apoptosis. Time-lapse fluorescent microscopy of FUCCI cell cycle probes transduced into aneuploid lung cancer cells revealed distinct fates of bipolar and polyploid cells after CDK2 inhibition. Apoptosis occurred in multipolar progeny but was repressed in persistent polyploid cancer cells. RNA-seq analyses after CDK2 inhibition of 4N versus 2N lung cancer cells were enriched for CDK1 pathway and KIF family members. The Cancer Genome Atlas (TCGA) analysis of lung cancers indicated CDK1 and KIF family member overexpression was associated with an unfavorable survival. Intravital microscopy of transplanted lung cancer cells in mice extended findings from the in vitro to in vivo settings. CDK2 inhibition of tumor-bearing mice produced polyploid cancer cells in vivo. These cancer cells were resistant to apoptosis and proliferated despite CDK2 inhibition. In contrast, polyploid populations were rarely detected in CDK2 inhibited human alveolar epithelial cells. These findings are translationally relevant. Combined targeting of CDK2 with CDK1 or kinesin family member antagonists should eliminate polyploid cancer cells, promote apoptosis and augment antineoplastic effects.

2025-04-06 | GSE292967 | GEO

The polyploid state plays a tumor suppressive role in the liver

Project description:Most cells in the liver are polyploid, but the functional role of polyploidy is unknown. We developed orthogonal mouse models to transiently and potently alter liver ploidy. Premature weaning, as well as knockdown of E2f8 or Anln, allowed us to toggle between diploid and polyploid states. While there was no impact of ploidy alterations on liver function, metabolism, or regeneration, more polyploid mice suppressed and more diploid mice accelerated tumorigenesis in mutagen and high-fat induced models. Mechanistically, the diploid state was more susceptible to Cas9-mediated tumor suppressor loss but was similarly susceptible to MYC oncogene activation, indicating that ploidy differentially protected the liver from distinct genomic aberrations.

2019-01-01 | GSE108645 | GEO

Karyotype analysis of polyploid Saccharomyces cerevisiae cell lines

Project description:The polyploid S. cerevisiae karyotypes were analyzed by array-CGH to identify the deletion or duplication of gene or chromosome during the strain construction and after experimental evolution.

2016-10-11 | GSE76595 | GEO

RNA expression profiles of murine polyploid trophoblast giant cells (TGCs) from day 9.5 implantation sites.

Project description:We employed RNA-seq to transcriptionally profile a pure population of hand-dissected polyploid TGCs from embryonic day 9.5. These data provide a set of polyploid-specific TGCs transcripts that will aid in the understanding of TGCs differentiation and endoreplication. TGCs were micro-dissected from day E9.5 nine implantation sites from C57BL/6J mice. The portion of the TGCs in direct contact with the spongiotrophoblast layer and the labyrinth layer were manually removed to avoid collecting any polyploid cells from the former or multi-nucleated syncytiotrophoblast cells from the latter.

2013-04-30 | E-GEOD-45782 | biostudies-arrayexpress

microRNA (miRNA) expression profiles of murine polyploid trophoblast giant cells (TGCs) from day 9.5 implantation sites.

Project description:We employed miRNA-seq to profile all miRNAs from a pure population of hand-dissected polyploid TGCs from embryonic day 9.5. These data set of polyploid-specific TGCs microRNAs will provide insights into TGCs differentiation and endoreplication. TGCs were micro-dissected from day E9.5 nine implantation sites from C57BL/J6 mice. The portion of the TGCs in direct contact with the spongiotrophoblast layer and the labyrinth layer were manually removed to avoid collecting any polyploid cells from the former or multi-nucleated syncytiotrophoblast cells from the latter.

2013-04-30 | E-GEOD-45784 | biostudies-arrayexpress

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