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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE273947 | GEO | 2025/03/26

REPOSITORIES: GEO

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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

Rac -dependent signaling from keratinocytes promotes differentiation of intradermal white adipocytes

Project description:Rac signaling affects numerous downstream targets; however, few studies have established in vivo levels using model animals. In the present study, wWe generated mice with a single knockout (KO) of Rac1 (Keratin5 (K5)-Cre;Rac1flox/flox, hereafter Rac1-KO) and double KO of Rac1 and Rac3 (K5-Cre;Rac1flox/flox;Rac3−/−, hereafter Rac1/Rac3-DKO) in keratinocytes. Hairless phenotype in Rac1-KO mice was markedly exacerbated in Rac1/Rac3-DKO mice. Notably, Rac1-KO mice also exhibited thinner dermal white adipose tissue, which was considerably further reduced in Rac1/Rac3-DKO mice. DNA microarray using primary keratinocytes from Rac1/Rac3-DKO mice exhibited decreased mRNA levels of Bmp2, Bmp5, Fgf20, Fgf21, Fgfbp1, and Pdgf-alpha. Combinational treatment with BMP2 and FGF21, BMP2 and FGF20, or PDGF and FGF21 in culture medium, but not individual purified recombinant proteins, could differentiate 3T3-L1 fibroblasts into adipocytes, as could culture media obtained from primary keratinocytes (both human and mouse). Conversely, addition of anti-BMP2 or anti-FGF21 antibodies into the culture medium inhibited fibroblast differentiation. Furthermore, combinational treatment with BMP2 and FGF21 promoted adipocyte differentiation only of rat primary white adipocyte precursors but not rat primary brown adipocyte precursors. Notably, brown adipogenesis by FGF21 was inhibited by BMP2. Thus, we here proposed a novel paracrine pathway from keratinocytes to intradermal pre-adipocytes using Rac1/Rac3-DKO mice, which is Rac-dependent and functions as an inducer of white adipocytes.

2019-11-06 | GSE122234 | GEO

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.

2020-06-26 | GSE100629 | GEO

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

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

| PRJNA1144139 | ENA

Rac3

Project description:Rattus norvegicus Rac3, Rac family small GTPase 3 [Source:RGD Symbol;Acc:1590052], is differentially expressed in 8 experiment(s);

| ENSRNOG00000048172 | ExpressionAtlas

RAC3

Project description:Monodelphis domestica RAC3, Rac family small GTPase 3 [Source:NCBI gene;Acc:100029873], is expressed in 2 baseline experiment(s);

| ENSMODG00000003244 | ExpressionAtlas

Rac3

Project description:Rattus norvegicus Rac3, Rac family small GTPase 3 [Source:RGD Symbol;Acc:1590052], is expressed in 2 baseline experiment(s);

| ENSRNOG00000048172 | ExpressionAtlas

SPIB promotes anoikis resistance via elevated autolysosomal process in lung cancer cells [RNA-seq]

Project description:Anoikis (detachment-induced cell death) is a specific type of programmed cell death which occurs in response to the loss of the correct extracellular matrix connections. Anoikis resistance is an important mechanism in cancer invasiveness and metastatic behavior. Autophagy, on the other hand, involves the degradation of damaged organelles and the recycling of misfolded proteins and intracellular components. However, the intersection of these two cellular responses in lung cancer cells has not been extensively studied. Here, we identified that upon matrix deprivation, the lymphocyte lineage-specific Ets transcription factor SPIB was activated and directly enhanced SNAP47 transcription in certain lung cancer cells. Loss of attachment-induced autophagy significantly increased anoikis resistance by SPIB activation. Consistent with this function, SPIB depletion by short hairpin RNA abrogated SNAP47 transcriptional activation upon matrix deprivation. Therefore, these data delineate an important role of SPIB in autophagy-mediated anoikis resistance in lung cancer cells. Accordingly, these findings suggest that manipulating SPIB-regulated pathways in vivo and evaluating the impact of anoikis resistance warrant further investigation.

2019-03-11 | GSE106592 | GEO

SPIB promotes anoikis resistance via elevated autolysosomal process in lung cancer cells [ChIP-seq]

2019-03-11 | GSE125561 | GEO

RAC3

Project description:Sus scrofa RAC3, Rac family small GTPase 3 [Source:VGNC Symbol;Acc:VGNC:92049], is differentially expressed in 1 experiment(s);

| ENSSSCG00000036973 | ExpressionAtlas