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Integrated analysis of the anoikis-related signature identifies RAC3 as a novel therapeutic target in hepatocellular carcinoma

ABSTRACT: Integrated analysis of the anoikis-related signature identifies RAC3 as a novel therapeutic target in hepatocellular carcinoma

PROVIDER: PRJNA1144139 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30126648_1.fastq.gz	Fastqsanger.gz
	SRR30126648_2.fastq.gz	Fastqsanger.gz
	SRR30126649_1.fastq.gz	Fastqsanger.gz
	SRR30126649_2.fastq.gz	Fastqsanger.gz
	SRR30126650_1.fastq.gz	Fastqsanger.gz

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Integrated analysis of the anoikis-related signature identifies RAC3 as a novel therapeutic target in hepatocellular carcinoma

Project description:Introduction: Anoikis is a form of programmed cell death. Anoikis resistance in hepatocellular carcinoma (HCC) promotes cancer cells shedding from the primary tumor site, thus contributing to survival and distant metastasis. However, the prognostic significance of anoikis-related genes (ARGs) and the biological functions of crucial genes in HCC have not been reported. Objectives: This study aimed to construct a model for predicting the outcome of patients with HCC based on ARGs and to investigate the clinicopathological significance and function of Rac family small GTPase 3 (RAC3) in HCC.

2025-05-07 | PXD057450 | Pride

Integrated analysis of the anoikis-related signature identifies RAC3 as a novel therapeutic target in hepatocellular carcinoma

2025-03-26 | GSE273947 | GEO

Adaptive anoikis resistance promotes ovarian cancer metastasis

Project description:Anoikis resistance or evasion of cell death triggered by cell detachment is a hallmark of cancer that is concurrent with cell survival and metastasis. Phenotypes of anoikis resistant cancer cells have been extensively investigated, however, how exposure to suspension stress may lead to acquisition of a anoikis resistance phenotype has not been previously described in detail. Here we show using a spectrum of ovarian cancer cells, that cycles of suspension stress followed by attached growth, leads to adaptation and acquisition of resistance to cell death in suspension . Comparing the stepwise transcriptomic changes as cells acquire resistance, we find strong transcriptional reprogramming in the population with a majority of differentially expressed genes being downregulated during progressive acquisition of anoikis resistance. Adapted anoikis resistant cells display an enhanced dependency on oxidative phosphorylation and are capable of evasion from T cell-mediated immune surveillance. We find that such acquired anoikis resistance is not genetic. However, transcriptional reprogramming is essential to this process as acquisition of such adaptive anoikis resistance invitro and invivo are both exquisitely sensitive to specific inhibition of transcriptional reprogramming. Our data demonstrate that recovery from the verge of anoikis leads to adaptation that promotes metastasis in ovarian cancer, but can be therapeutically prevented by specific inhibitors to transcriptional reprogramming.

2024-12-01 | GSE241546 | GEO

Gene Signature to Identify Vascular Invasion in Hepatocellular Carcinoma

Project description:Background: The presence of vascular invasion (VI) in pathology specimens has been widely described as closely linked to poor outcome in hepatocellular carcinoma (HCC) patients after tumor resection. Previous attempts have been conducted to achieve molecular markers or signatures to predict HCC recurrence in HCC. Here, we aim to develop a diagnostic model combining clinical and genomic variables able to detect the presence of VI prior to surgery and link it to survival estimation. Methods: Seventy-nine HCV related HCC samples from patients that underwent surgical resection as a treatment for HCC were subjected to Genome-wide gene expression profiling and a predictive model of vascular invasion was constructed. The model was tested in an independent-validation set of 153 fixed tissue samples of resected HCC. Quantitative RTPCR and inmunohistochemistry were performed in HCC samples to test a potential biomarker. Results: A 39-gene signature was able to accurately (72%) identify vascular invasion in HCC patients treated with resection. A model including tumor size and the signature is able to predict presence of VI with 85% accuracy in HCV-related HCC patients, and is able to exclude VI in up to 87% cases in HCC from all etiologies. Conclusions: Using the VI gene signature together with tumor size, VI can be successfully detected in HCC patients. The diagnostic model, integrated in a previously reported survival chart is able to provide an estimated survival for selected cases. Clinical implications of this fact are relevant to provide objective data to further apply expanded indication of curative treatments in HCC. Gene-expression profiling was performed using formalin-fixed, paraffin-embedded hepatocellular carcinoma tissues obtained at the time of surgical resection.

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Gene Signature to Identify Vascular Invasion in Human Hepatocellular Carcinoma

Project description:This SuperSeries is composed of the following subset Series: GSE9843: Gene expression profiling of 91 hepatocellular carcinomas with hepatitis C virus etiology, Samples with "vascular invasion: Yes/No" were included in the study. GSE20017: Gene Signature to Identify Vascular Invasion in Hepatocellular Carcinoma Refer to individual Series

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Gene expression signatures in anoikis-resistance of human prostate PC-3 cells

Project description:To investigate potential molecular targets that regulate metastasis and metabolism in anoikis-resistance of prostate cancer cells, we have establised anoikis-resistant prostate PC-3 cells with ultra-low attachment 6-well plates (Corning) and employed whole genome microarray expression profiling as a discovery platform to identify differentially expressed genes between anoikis-resistant PC-3 cells and corresponding parental cells.

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