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SMARCA4 loss-of-function induces cisplatin resistance to activate YAP1-dependent epithelial-to-mesenchymal in triple negative breast cancer

ABSTRACT: SMARCA4 loss-of-function induces cisplatin resistance to activate YAP1-dependent epithelial-to-mesenchymal in triple negative breast cancer

PROVIDER: PRJNA739566 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14870088_1.fastq.gz	Fastqsanger.gz
	SRR14870088_2.fastq.gz	Fastqsanger.gz
	SRR14870089_1.fastq.gz	Fastqsanger.gz
	SRR14870089_2.fastq.gz	Fastqsanger.gz
	SRR14870090_1.fastq.gz	Fastqsanger.gz

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SMARCA4 loss-of-function induces cisplatin resistance to activate YAP1-dependent epithelial-to-mesenchymal in triple negative breast cancer

Project description:We report transcriptome profiling (RNA-seq) for SMARA4 knock-out to elucidate the association with cisplatin-resistance and SMARCA4 loss-of-function using triple negative breast cancer cell lines.

2021-11-17 | GSE178532 | GEO

Project description:SMARCA4 inactivation induces cisplatin resistance to activate YAP1-dependent epithelial-to-mesenchymal in triple negative breast cancer

| PRJNA739039 | ENA

Olaparib resistance and cisplatin responses in triple negative breast cancer

Project description:PARP inhibitor and platinum based drugs such as cisplatin are promising therapies for triple negative breast cancer and exploit the deficiencies in BRCA1 or BRCA2, or homologous recombination repair defects. However, PARP inhibitor resistance is proven to be a major clinical problem. Acquired PARP inhibitor resistance has been linked with co-resistance to platinum-based drugs. To determine how acquired olaparib resistance affects cisplatin response and whether this is influenced by their BRCA1 status, we performed RNAseq transcriptome analysis of isogenic triple negative breast cancer models of olaparib resistance with normal and mutant BRCA1.

2021-07-22 | GSE165914 | GEO

SMARCA4 Depletion Induces Cisplatin Resistance by Activating YAP1-Mediated Epithelial-to-Mesenchymal Transition in Triple-Negative Breast Cancer.

Project description:The role of SMARCA4, an ATPase subunit of the SWI/SNF chromatin remodeling complex, in genomic organization is well studied in various cancer types. However, its oncogenic role and therapeutic implications are relatively unknown in triple-negative breast cancer (TNBC). We investigated the clinical implication and downstream regulation induced by SMARCA4 inactivation using large-scale genome and transcriptome profiles. Additionally, SMARCA4 was knocked out in MDA-MB-468 and MDA-MB-231 using CRISPR/Cas9 to identify gene regulation and a targetable pathway. First, we observed an increase in SMARCA4 mutations in cisplatin resistance and metastasis in TNBC patients. Its inactivation was associated with the mesenchymal-like (MSL) subtype. Gene expression analysis showed that the epithelial-to-mesenchymal transition (EMT) pathway was activated in SMARCA4-deficient patients. Next, the Hippo pathway was activated in the SMARCA4 inactivation group, as evidenced by the higher CTNNB1, TGF-β, and YAP1 oncogene signature scores. In SMARCA4 knockout cells, EMT was upregulated, and the cell line transcriptome changed from the SL to the MSL subtype. SMARCA4 knockout cells showed cisplatin resistance and Hippo-YAP/TAZ target gene activation. The YAP1 inhibitor verteporfin suppressed the expression of YAP1 target genes, and decreased cell viability and invasiveness on SMARCA4 knockout cells. SMARCA4 inactivation in TNBC endowed the resistance to cisplatin via EMT activation. The YAP1 inhibitor could become a novel strategy for patients with SMARCA4-inactivated TNBC.

| S-EPMC8582548 | biostudies-literature

Cisplatin-induced gene expression changes in triple-negative breast cancer (TNBC) cells

Project description:Breast cancers lacking receptors for estrogen, progesterone or HER2 on their cell surface are called triple-negative breast cancers (TNBCs). TNBCs account for ~15-20% of all invasive breast cancers and do not benefit from anti-hormonal or anti-HER2 treatments. Although patients with TNBC can initially respond to chemotherapy, they do have worse overall prognosis compared to other breast cancer subtypes. Unfortunately, TNBCs lack clear targetable ‘driver’ oncogenes. Thus, there is an unmet need for strategies to improve the therapeutic options for these patients. We used microarrays to assess differences in gene expression in triple-negative breast cancer cells in response to the platinum-based chemotherapeutic agent cisplatin. The purpose was to find drug induced changes in gene expression level that could differentiate cisplatin sensitive from cisplatin resistant TNBC cell lines.

2017-08-26 | GSE103115 | GEO

Effect of depletion of YAP1 on gene expression in triple negative breast cancer

Project description:To investigate the cooperative function HJURP/YAP1/NDRG1 in the regulation of progression in triple negative breast cancer, we established MDA-MB-231 cell lines in which each target gene has been knocked down by shRNA. We then performed gene expression profiling analysis using data obtained from RNA-seq of 2 different cells.

2022-10-24 | GSE201877 | GEO

Tumor expression data from neoadjuvant trial of cisplatin monotherapy in triple negative breast cancer patients

2009-11-04 | GSE18864 | GEO

Tumor expression data from neoadjuvant trial of cisplatin monotherapy in triple negative breast cancer patients

Project description:Evidence suggests that BRCA1 mutation associated tumors have increased sensitivity to DNA damaging agents like cisplatin. Sporadic triple negative breast cancers (TNBC) have many phenotypic similarities to BRCA1 tumors and may have a similar sensitivity to cisplatin. We tested the efficacy of cisplatin monotherapy in 28 TNBC patients in a single arm neoadjuvant trial with outcome measured by pathologic treatment response quantified using the Miller-Payne scale. We used microarrays gene expression profiles to determine tumor subtype of each trial tumor sample and to test various expression signatures for association with pathologic response to cisplatin. Pretreatment tumor samples from the clinical trial (N=24 with adequate tissue) were used for RNA extraction, linear amplification, biotin labeling and hybridization to Affymetrix U133 plus 2.0 arrays. A reference set of 51 primary breast tumors representing all subtypes of breast cancer were processed in a similar manner to include linear amplification, and hybridized to Affymetrix arrays.

2009-11-04 | E-GEOD-18864 | biostudies-arrayexpress

Effect of SMARCA4 degradation on ID8 ovarian cancer cells senescent and not senescent.

Project description:We report the analysis of RNA sequencing aimed at understanding the effects induced by AU-15330 (SMARCA4 PROTAC)-mediated degradation of SMARCA4 in P53-deficient senescent ID8 ovarian tumour cells. Specifically, we focus on exploring the repercussions of inhibiting SMARCA4, a constituent of the SWI/SNF complex subunit, on the SASP and immune activity within cisplatin-treated senescent cancer cells. The findings will help characterise the role of SMARCA4 inhibition on senescence surveillance by Natural Killer cells.

2024-09-19 | GSE249062 | GEO

SOX4 AND SMARCA4 COOPERATIVELY REGULATE PI3K SIGNALING THROUGH TRANSCRIPTIONAL ACTIVATION OF TGFBR2 IN TRIPLE NEGATIVE BREAST CANCER

Project description:Dysregulation of PI3K/Akt signaling is a dominant feature in basal-like or triple-negative breast cancers (TNBC). However, the mechanisms regulating this pathway are largely unknown in this subset of aggressive tumors. Here we demonstrate that the transcription factor SOX4 is a key regulator of PI3K signaling in TNBC. Genomic and proteomic analyses coupled with mechanistic studies identified TGFBR2 as a direct transcriptional target of SOX4 and demonstrated that TGFBR2 is required to mediate SOX4-dependent PI3K signaling. We further report that SOX4 and the SWI/SNF ATPase SMARCA4, which are uniformly overexpressed in basal-like tumors, form a previously unreported complex that is required to maintain an open chromatin conformation at the TGFBR2 regulatory regions in order to mediate TGFBR2 expression and PI3K signaling. Collectively, our findings delineate the mechanism by which SOX4 and SMARCA4 cooperatively regulate PI3K/Akt signaling and suggest that this complex may play an essential role in TNBC genesis and/or progression. Kinase enrichment proteomic analysis was performed using HCC1143 breast cancer cells treated with a control siRNA pool or a pool targeting SOX4 in biological triplicate to evaluate the effects on the functional kinome.

2021-03-03 | PXD022596 | Pride

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