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The FAK-Inhibitor BI 853520 exerts anti-tumor effects in breast cancer

ABSTRACT: The FAK-Inhibitor BI 853520 exerts anti-tumor effects in breast cancer

PROVIDER: PRJNA477312 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7406060_1.fastq.gz	Fastqsanger.gz
	SRR7406060_2.fastq.gz	Fastqsanger.gz
	SRR7406061_1.fastq.gz	Fastqsanger.gz
	SRR7406061_2.fastq.gz	Fastqsanger.gz
	SRR7406062_1.fastq.gz	Fastqsanger.gz

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The FAK-Inhibitor BI 853520 exerts anti-tumor effects in breast cancer

Project description:In order to delineate the molecular mechanisms leading to the therapeutic effect of BI 853520 on primary tumor growth, mice harboring 4T1 primary tumors were treated for five days with BI 853520, and RNA extracted from total tumors was subjected to next generation sequencing. Only primary tumors with sufficient RNA quality were included into further analysis (Suppl. Fig. 2A). Gene expression correlation analysis displayed a clear separation of transcriptomic profiles derived from primary tumors of mice treated with BI 853520 or vehicle (Suppl. Fig. 2B). Comparative gene expression analysis of primary tumors of mice treated with BI 853520 versus vehicle control revealed 1293 upregulated and 475 downregulated genes (cutoffs: p-value ≤ 0.05, fold change +/- 1.5). Functional enrichment analysis for biological processes and signaling pathways indicated that the regulation of epithelial cell proliferation, positive regulation of cell cycle/cell proliferation/cell division and regulation of cell proliferation/cell division/cell growth were enriched in genes downregulated by BI 853520 treatment (Fig. 3A). In line with this finding, gene set enrichment analysis confirmed a significant reduction in the relative expression of genes important for cell cycle and positive regulation of mitotic cell cycle (including cyclin-dependent kinase 1 and 4; Cdk1: log2 fold-change= -0.4519, FDR= 4.24e-03; Cdk4: log2 fold-change= -0.3072, FDR= 0.003718), while the negative regulation of cell proliferation was increased following BI 853520 treatment (Fig. 3C; Suppl. Fig. 2C).

2019-07-19 | GSE116117 | GEO

BRD4 inhibitor GNE987 exerts anti-cancer effects in Neuroblastoma

Project description:BRD4 inhibitor GNE987 exerts anti-cancer effects in Neuroblastoma

| PRJNA785569 | ENA

BRD4 inhibitor MZ1 exerts anti-cancer effects in Neuroblastoma

Project description:BRD4 inhibitor MZ1 exerts anti-cancer effects in Neuroblastoma

| PRJNA797669 | ENA

BRD4 inhibitor GNE987 exerts anti-cancer effects in Osteosarcoma

Project description:BRD4 inhibitor GNE987 exerts anti-cancer effects in Osteosarcoma

| PRJNA1019364 | ENA

The FAK inhibitor BI 853520 exerts anti-tumor effects in breast cancer.

Project description:Focal adhesion kinase (FAK) is a cytoplasmic tyrosine kinase that regulates a plethora of downstream signaling pathways essential for cell migration, proliferation and death, processes that are exploited by cancer cells during malignant progression. These well-established tumorigenic activities, together with its high expression and activity in different cancer types, highlight FAK as an attractive target for cancer therapy. We have assessed and characterized the therapeutic potential and the biological effects of BI 853520, a novel small chemical inhibitor of FAK, in several preclinical mouse models of breast cancer. Treatment with BI 853520 elicits a significant reduction in primary tumor growth caused by an anti-proliferative activity by BI 853520. In contrast, BI 853520 exerts effects with varying degrees of robustness on the different stages of the metastatic cascade. Together, the data demonstrate that the repression of FAK activity by the specific FAK inhibitor BI 853520 offers a promising anti-proliferative approach for cancer therapy.

| S-EPMC6148276 | biostudies-literature

BRD4 inhibitor GNE987 exerts anti-cancer effects in Neuroblastoma (ChIP-Seq)

Project description:BRD4 inhibitor GNE987 exerts anti-cancer effects in Neuroblastoma (ChIP-Seq)

| PRJNA800647 | ENA

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.

2019-10-31 | GSE139604 | GEO

Synergism of FAK and ROS1 inhibitors in the treatment of CDH1-deficient cancers mediated by FAK-YAP-TRX signaling

Project description:To investigate the ROS1 and FAK inhibitors combination may provide stronger anti-cancer effects by targeting CDH1 deficiency and potentially overcome drug resistance. Here, we evaluated the effects and mechanisms of combined treatment with FAK inhibitor IN10018 and ROS1 inhibitors.

2024-12-01 | GSE229195 | GEO

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

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

| PRJNA580469 | ENA

ERK5 suppression overcomes FAK inhibitor resistance in mutant KRAS-driven non-small cell lung cancer [p826_PND_A549]

Project description:Mutated KRAS serves as the oncogenic driver in 30% of non-small cell lung cancers (NSCLCs) and is associated with metastatic and therapy-resistant tumors. Focal Adhesion Kinase (FAK) acts as a mediator in sustaining KRAS-driven lung tumors, and although FAK inhibitors are currently undergoing clinical development, clinical data indicated that their efficacy in producing long-term anti-tumor responses is limited. Here we revealed two FAK interactors, extracellular-signal-regulated kinase 5 (ERK5) and cyclin-dependent kinase 5 (CDK5) as key players underlying FAK-mediated maintenance of KRAS mutant NSCLC. Inhibition of ERK5 and CDK5 synergistically suppressed FAK function, decreased proliferation and induced apoptosis owing to exacerbated ROS-induced DNA damage. Accordingly, concomitant pharmacological inhibition of ERK5 and CDK5 in a mouse model of KrasG12D-driven lung adenocarcinoma suppressed tumor progression and promoted cancer cell death. Cancer cells resistant to FAK inhibitors showed enhanced ERK5-FAK signaling dampening DNA damage. Notably, ERK5 inhibition prevents resistance to FAK inhibitors, significantly enhancing the efficacy of antitumor responses. Therefore, we propose ERK5 inhibition as a potential co-targeting strategy to counteract FAK inhibitor resistance in NSCLC.

2024-09-16 | GSE255643 | GEO

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