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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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			Action	DRS
	SRR8822580_1.fastq.gz	Fastqsanger.gz
	SRR8822580_2.fastq.gz	Fastqsanger.gz
	SRR8822590_1.fastq.gz	Fastqsanger.gz
	SRR8822590_2.fastq.gz	Fastqsanger.gz
	SRR8822581_1.fastq.gz	Fastqsanger.gz

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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.

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

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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

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

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

Project description:Gene copy number alterations, tumor cell stemness, and the development of platinum chemotherapy resistance contribute to high-grade serous ovarian cancer (HGSOC) recurrence. Stem phenotypes involving Wnt-β-catenin, aldehyde dehydrogenase activities, intrinsic platinum resistance, and tumorsphere formation are here associated with spontaneous gains in Kras, Myc and FAK (KMF) genes in a new aggressive murine model of ovarian cancer. Adhesion-independent FAK signaling sustained KMF and human tumorsphere proliferation as well as resistance to cisplatin cytotoxicity. Platinum-resistant tumorspheres can acquire a dependence on FAK for growth. Accordingly, increased FAK tyrosine phosphorylation was observed within HGSOC patient tumors surviving neo-adjuvant chemotherapy. Combining a FAK inhibitor with platinum overcame chemoresistance and triggered cell apoptosis. FAK transcriptomic analyses across knockout and reconstituted cells identified 135 targets, elevated in HGSOC, that were regulated by FAK activity and β-catenin including Myc, pluripotency and DNA repair genes. These studies reveal an oncogenic FAK signaling role supporting chemoresistance.

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We performed gene expression profiles of human bronchoalveolar epithelial cells (HBEC) transduced with GFP labeled murine focal adhesion kinase (PMX-Purom-GFP-mFAK) or GFP control empty vector counterpart (PMX-Purom-GFP-empty)

Project description:The goal if this project was to determine the cellular pathways affected by FAK protein overexpression downstream of oncogenic KRAS and RHOA in normal lung epithelium. In addition, we aim to characterize the potential downstream modulators of cell growth and migration upon FAK hyperactivation. We identified pathways in DNA damage, cell growth, apoptosis and cytoskeleton remodeling pertaining to tissue differentiation and carcinogenesis signature respectively. For this study, two duplicate samples were analyzed in triplicate arrays for a total of 6 data poinst per condition. The groups compared were PMX-Purom-GFP-mFAK against PMX-Purom-GFP-emty.

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Next generation sequencing comparing effects of FFSS, FAK inhibitor and FAK gene deletion.

Project description:Purpose: The goals of this study are to compare the effect of FFSS, FAK inhibitor, and FAK gene deletion on gene expression of NGS-derived RNA-sequencing.

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

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