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Knockdown of ribosome RNA processing protein 15 (RRP15) suppresses metastasis of hepatocellular carcinoma via LAMC2/FAK pathway

ABSTRACT: Collectively, RRP15 is highly expressed in HCC tissues and is positively correlated with OS% and DSS% of HCC patients. Knockdown of RRP15 notably prevented the proliferation of HCC cells in vitro and the growth of ectopic transplanted tumors in vivo. Moreover, RRP15 knockdown suppressed the cells migration, invasion and adhesion through reducing the activation of laminin 5/integrin β4/FAK signaling pathway. The findings of the current study revealed the role of RRP15 in the progression of HCC, and laid a theoretical basis for RRP15 as a potential target for HCC diagnosis or/and treatment.

ORGANISM(S): Homo sapiens

PROVIDER: GSE228416 | GEO | 2024/03/20

REPOSITORIES: GEO

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TMTC1 promotes invasiveness of ovarian cancer

Project description:Ovarian cancer is the most lethal gynecological malignancy and is characterized by peritoneal disseminated metastasis. Although O-mannosyltransferase TMTC1 is highly expressed by ovarian cancer, its pathophysiologic role in ovarian cancer remains unclear. Here, immunohistochemistry showed that TMTC1 was overexpressed in ovarian cancer tissues compared with the adjacent non-tumor ovarian tissues and high TMTC1 expression was associated with poor prognosis in patients with ovarian cancer. Silencing TMTC1 reduced ovarian cancer cell viability, migration, and invasion in vitro as well as suppressed peritoneal tumor growth and metastasis in vivo. Moreover, TMTC1 knockdown reduced cell-laminin adhesion, which was associated with the decreased phosphorylation of FAK at pY397. Conversely, TMTC1 overexpression promoted these malignant properties in ovarian cancer cells. Glycoproteomic analysis and Concanavalin A (ConA) pull-down assays showed that integrins β1 and β4 were novel O-mannosylated protein substrates of TMTC1. Furthermore, TMTC1-mediated cell migration and invasion were significantly reversed by siRNA-mediated knockdown of integrin β1 or β4. Collectively, these results suggest that TMTC1-mediated invasive behaviors are primarily through integrins β1 and β4 and that TMTC1 is a potential therapeutic target for ovarian cancer.

2023-10-24 | PXD037907 | Pride

Genome wide gene expression profile of pancreatic ductal adenocarcinoma (PDAC) cells after knock down of focal adhesion kinase (FAK).

Project description:In our experiments, we showed that FAK regulates PDAC clonogenicity and selfrenewal. In order to evaluate the impact of FAK knockdown on the transcriptomes of PDAC , we knocked down FAK in two PDAC cell lines and compared the gene expression signatures with the cancer stem cell (CSC)associated gene signatures by GSEA analysis. CCS related gene profile was inversely related with FAK-knockdown gene signature.

2017-04-20 | GSE97488 | 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

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

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

pCMV-FRNK/pCMV-FAK vs pCMV-FAK in CTL

Project description:CMV-driven inhibition of FAK in soleus muscle was compared vs contralateral muscle

2009-12-31 | GSE12744 | GEO

siRNA profiling if human MCF-7 cell line to investigate the role of FAK, dominant-negative FAK, FAK-CD and FAKsiRNA in MCF-7 human breast cancer cell tumorigenesis

2009-08-22 | E-GEOD-11581 | biostudies-arrayexpress

Effect of norepinephrine and focal adhesion kinase (FAK) knockdown in prostate cancer

Project description:Chronic stress is associated with hormonal alterations that are known to promote cancer progression. The stress hormone norepinephrine promotes migration and metastasis of prostate cancer cells. Focal adhesion kinase (FAK) is a non-receptor protein tyrosine kinase which is phosphorylated during chronic stress or norepinephrine treatment. Here, we investigated how norepinephrine modulates the gene expression in Myc-CaP prostate cancer cell line. We also focused on the effect of FAK knockdown in norepinephrine-induced changes of the gene expression profile.

2018-08-29 | GSE119157 | GEO

Gene profile of breast cancer tumors with low and high FAK expression

Project description:The gene expression profiles were identified in breast cancer tumors with different level of FAK three tumors with low FAK expression identified by IHC and 3 tumors with high FAK expression. 2 triple-negative with low and one triple negative with high FAK expression was among these 6 samples

2014-02-01 | E-GEOD-53618 | biostudies-arrayexpress

Transcriptome analysis of rat soleus muscle after altered loading state and somatic overexpression of FAK

Project description:This SuperSeries is composed of the following subset Series: GSE12743: pCMV-FAK vs pCMV in CTL GSE12744: pCMV-FRNK/pCMV-FAK vs pCMV-FAK in CTL GSE12745: pCMV-FAK vs pCMV in HU GSE12746: pCMV-FAK vs pCMV in R1 GSE12747: pCMV-FAK vs pCMV in R5 Refer to individual Series

2009-12-30 | E-GEOD-16466 | biostudies-arrayexpress

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