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

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

PROVIDER: PRJNA949657 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23995906_1.fastq.gz	Fastqsanger.gz
	SRR23995906_2.fastq.gz	Fastqsanger.gz
	SRR23995907_1.fastq.gz	Fastqsanger.gz
	SRR23995907_2.fastq.gz	Fastqsanger.gz
	SRR23995908_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

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

Project description: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.

2024-03-20 | GSE228416 | GEO

Knockdown of ribosome RNA processing protein 15 suppresses migration of hepatocellular carcinoma through inhibiting PATZ1-associated LAMC2/FAK pathway.

Project description:BackgroundRibosomal RNA processing protein 15 (RRP15) has been found to regulate the progression of hepatocellular carcinoma (HCC). Nevertheless, the extent to which it contributes to the spread of HCC cells remains uncertain. Thus, the objective of this research was to assess the biological function of RRP15 in the migration of HCC.MethodsThe expression of RRP15 in HCC tissue microarray (TMA), tumor tissues and cell lines were determined. In vitro, the effects of RRP15 knockdown on the migration, invasion and adhesion ability of HCC cells were assessed by wound healing assay, transwell and adhesion assay, respectively. The effect of RRP15 knockdown on HCC migration was also evaluated in vivo in a mouse model.ResultsBioinformatics analysis showed that high expression of RRP15 was significantly associated with low survival rate of HCC. The expression level of RRP15 was strikingly upregulated in HCC tissues and cell lines compared with the corresponding controls, and TMA data also indicated that RRP15 was a pivotal prognostic factor for HCC. RRP15 knockdown in HCC cells reduced epithelial-to-mesenchymal transition (EMT) and inhibited migration in vitro and in vivo, independent of P53 expression. Mechanistically, blockade of RRP15 reduced the protein level of the transcription factor POZ/BTB and AT hook containing zinc finger 1 (PATZ1), resulting in decreased expression of the downstream genes encoding laminin 5 subunits, LAMC2 and LAMB3, eventually suppressing the integrin β4 (ITGB4)/focal adhesion kinase (FAK)/nuclear factor κB kappa-light-chain-enhancer of activated B cells (NF-κB) signaling pathway.ConclusionsRRP15 promotes HCC migration by activating the LAMC2/ITGB4/FAK pathway, providing a new target for future HCC treatment.

| S-EPMC10936014 | biostudies-literature

Coupled protein synthesis and ribosome-guided piRNA processing on mRNAs

Project description:Coupled protein synthesis and ribosome-guided piRNA processing on mRNAs

| PRJNA649449 | ENA

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

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

Hierarchical RNA processing is rate limiting for mitochondrial ribosome assembly

Project description:In animals the organization of the compact mitochondrial genome and lack of introns have necessitated a unique mechanism for RNA processing. To date the regulation of mitochondrial RNA processing and its importance for ribosome biogenesis and energy metabolism are not clear. To understand the in vivo role of the endoribonuclease component of the RNase P complex, MRPP3, we created conditional knockout mice. Here we show that MRPP3 is essential for life, and heart and skeletal muscle-specific knockout leads to a cardiomyopathy early in life, indicating that it is the only RNase P enzyme in mitochondria. We show that RNA processing is required for the biogenesis of the respiratory chain and mitochondrial function. Transcriptome-wide parallel analyses of RNA ends (PARE) and RNA-Seq enabled us to identify the in vivo cleavage sites of RNase P. Cleavage of the 5â² tRNA ends precedes 3â² end processing in vivo and is required for the correct biogenesis of the mitochondrial ribosomal subunits and mitoribosomal proteins that are differentially stabilized or degraded in the absence of mature rRNAs. Finally we identify that large mitoribosomal proteins can form a subcomplex on a precursor mt-RNA containing the 16S rRNA indicating that mitoribosomal biogenesis proceeds co-transcriptionally. Taken together our data show that RNA processing links transcription to translation via assembly of the mitoribosome. Total RNA was isolated from heart tissue from 11 week old control (Mrpp3loxP/loxP) and Mrpp3 knockout mice (Mrpp3loxP/loxP, +/Ckmm), TruSeq libraries produced in triplicate, sequenced and analysed for differential expression. Mitochondrial RNA was isolated from heart tissue from 11 week old control (Mrpp3loxP/loxP) and Mrpp3 knockout mice (Mrpp3loxP/loxP, +/Ckmm), PARE libraries produced in triplicate and sequenced for analysis of mitochondrial RNA processing.

2016-08-04 | E-GEOD-83471 | biostudies-arrayexpress

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

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

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