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FAK activity sustains intrinsic and acquired ovarian cancer resistance to platinum chemotherapy [KMF parental, KMF clone KT13 (FAK-/-), KT13 + GFP-FAK, KT13 + GFP-FAK R454, and KT13 + deltaGSK beta-catenin]

ABSTRACT: FAK activity sustains intrinsic and acquired ovarian cancer resistance to platinum chemotherapy [KMF parental, KMF clone KT13 (FAK-/-), KT13 + GFP-FAK, KT13 + GFP-FAK R454, and KT13 + deltaGSK beta-catenin]

PROVIDER: PRJNA530132 | ENA |

REPOSITORIES: ENA

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FAK activity sustains intrinsic and acquired ovarian cancer resistance to platinum chemotherapy [KMF parental, KMF clone KT13 (FAK-/-), KT13 + GFP-FAK, KT13 + GFP-FAK R454, and KT13 + deltaGSK beta-catenin]

Project description:Gene copy number changes, cancer stem cell (CSC) increases, and platinum chemotherapy resistance contribute to poor prognosis in patients with recurrent high grade serous ovarian cancer (HGSOC). CSC phenotypes involving Wnt-b-catenin and aldehyde dehydrogenase activities, platinum resistance, and tumor initiating frequency are here associated with spontaneous genetic gains, including genes encoding KRAS, MYC and FAK, in a new murine model of ovarian cancer (KMF). Noncanonical FAK signaling was sufficient to sustain human and KMF tumorsphere proliferation, CSC survival, and platinum resistance. Increased FAK tyrosine phosphorylation occurred in HGSOC patient tumors surviving neo-adjuvant platinum and paclitaxel chemotherapy and platinum resistant tumorspheres acquired FAK dependence for growth. Importantly, combining a pharmacologic FAK inhibitor with platinum overcame chemoresistance and triggered apoptosis in vitro and in vivo. Knockout, rescue, genomic and transcriptomic analyses collectively identified more than 400 genes regulated along a FAK/b-catenin/Myc axis impacting stemness and DNA repair in HGSOC, with 66 genes gained in a majority of Cancer Genome Atlas samples. Together, these results support combinatorial testing of FAK inhibitors for the treatment of recurrent ovarian cancer.

2019-07-01 | GSE129098 | GEO

FAK activity sustains intrinsic and acquired ovarian cancer resistance to platinum chemotherapy [ID8 and ID8-IP / KMF cells]

2019-07-01 | GSE129097 | GEO

FAK activity sustains intrinsic and acquired ovarian cancer resistance to platinum chemotherapy

Project description:FAK activity sustains intrinsic and acquired ovarian cancer resistance to platinum chemotherapy

| PRJNA530129 | ENA

FAK activity sustains intrinsic and acquired ovarian cancer resistance to platinum chemotherapy [ID8 and ID8-IP / KMF cells]

Project description:FAK activity sustains intrinsic and acquired ovarian cancer resistance to platinum chemotherapy [ID8 and ID8-IP / KMF cells]

| PRJNA530133 | ENA

FAK activity sustains intrinsic and acquired ovarian cancer resistance to platinum chemotherapy.

Project description: Not available

| S-EPMC6721800 | biostudies-literature

FAK activity sustains intrinsic and acquired ovarian cancer resistance to platinum chemotherapy

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-07-01 | GSE129099 | GEO

Platinum Genomes

Project description:Platinum Genomes

| PRJNA347414 | ENA

Identification of the possible molecules by which acquired platinum resistance induces EMT-like changes in urothelial carcinoma

Project description:To identify the possible targets in EMT-acquisition after developing acquired platinum resistance in urothelial carcinoma (UC), we examined the changes in global gene expression before and after development of acquired platinum resistance. Comparing two types of acquired platinum resistant UC cells and their corresponding parent cells, in the end we identified 49 genes (25 up-regulated and 24 down-regulated genes) which were commonly changed in two acquired platinum resistant UC cells. Four invasive UC cell lines, T24, 5637, and those acquired platinum-resistant sublines T24PR and 5637PR, were used for microarrays. T24PR and 5637PR cells were newly established in our laboratory, which were grown and passaged upon reaching confluence in medium containing CDDP over a 6-month period. In preliminary studies, we found that these cell lines had an altered phenotype with morphologic and molecular changes consistent with EMT, and exhibited a marked difference in migratory potential before and after developing platinum resistance.

2016-07-01 | E-GEOD-58624 | biostudies-arrayexpress

Identification of the possible molecules by which acquired platinum resistance induces EMT-like changes in urothelial carcinoma

2016-07-01 | GSE58624 | GEO

Role of FAK, dominant-negative FAK, FAK-CD and FAKsiRNA in MCF-7 human breast cancer cell tumorigenesis

Project description:Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase that plays an important role in proliferation, motility, adhesion, invasion, angiogenesis, and survival signaling. Focal adhesion kinase has been shown to be overexpressed in many types of tumors, including breast cancer at early stages of tumorigenesis. To study the biological role of FAK in breast tumorigenesis, we used FAKsiRNA to down-regulate FAK in MCF-7 cell lines.

2009-08-17 | GSE11581 | GEO

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