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LINC01133 promotes pancreatic ductal adenocarcinoma epithelial-mesenchymal transition mediated by SPP1 through binding to Arp3

ABSTRACT: LINC01133 promotes pancreatic ductal adenocarcinoma epithelial-mesenchymal transition mediated by SPP1 through binding to Arp3

PROVIDER: PRJNA1112428 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29060188.fastq.gz	Fastqsanger.gz
	SRR29060189.fastq.gz	Fastqsanger.gz
	SRR29060190.fastq.gz	Fastqsanger.gz
	SRR29060191.fastq.gz	Fastqsanger.gz
	SRR29060192.fastq.gz	Fastqsanger.gz

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LINC01133 promotes pancreatic ductal adenocarcinoma epithelial-mesenchymal transition mediated by SPP1 through binding to Arp3

Project description:Pancreatic ductal adenocarcinoma (PDAC) is a lethal disease with limited treatment methods. Long non-coding RNAs (lncRNAs) have been found involved in tumorigenic and progression. The present study revealed that LINC01133, a fewly reported lncRNA, was one of 16 hub genes that could predict PDAC patients' prognosis. LINC01133 was over-expressed in PDAC tumors compared to adjacent pancreas, and could promote PDAC proliferation and metastasis in vitro and in vivo, as well as inhibited PDAC apoptosis. LINC01133 expression positively correlated to secreted phosphoprotein 1 (SPP1) expression, leading to an enhanced epithelial-mesenchymal transition (EMT) process. LINC01133 bound with actin-related protein 3 (Arp3), the complex reduced SPP1 mRNA degradation which increased SPP1 mRNA level, ultimately leading to PDAC proliferation. This research revealed a novel mechanism of PDAC development and provided a potential prognosis indicator that may benefit PDAC patients.

2024-07-17 | GSE267702 | GEO

LINC01133 promotes pancreatic ductal adenocarcinoma epithelial-mesenchymal transition mediated by SPP1 through binding to Arp3.

Project description:Pancreatic ductal adenocarcinoma (PDAC) is a lethal disease with limited treatment methods. Long non-coding RNAs (lncRNAs) have been found involved in tumorigenic and progression. The present study revealed that LINC01133, a fewly reported lncRNA, was one of 16 hub genes that could predict PDAC patients' prognosis. LINC01133 was over-expressed in PDAC tumors compared to adjacent pancreas and could promote PDAC proliferation and metastasis in vitro and in vivo, as well as inhibit PDAC apoptosis. LINC01133 expression positively correlated to secreted phosphoprotein 1 (SPP1) expression, leading to an enhanced epithelial-mesenchymal transition (EMT) process. LINC01133 bound with actin-related protein 3 (Arp3), the complex reduced SPP1 mRNA degradation which increased SPP1 mRNA level, ultimately leading to PDAC proliferation. This research revealed a novel mechanism of PDAC development and provided a potential prognosis indicator that may benefit PDAC patients.

| S-EPMC11237081 | biostudies-literature

Pancreatic ductal adenocarcinoma

Project description:Pancreatic ductal adenocarcinoma

| PRJNA432344 | ENA

SAMD1 suppresses epithelial-mesenchymal transition pathways in pancreatic ductal adenocarcinoma

Project description:SAMD1 suppresses epithelial-mesenchymal transition pathways in pancreatic ductal adenocarcinoma

| PRJNA999235 | ENA

RNA-sequencing of HGC27 cells with and without linc01133 overexpression

Project description:The long intergenic non-coding RNA linc01133 is reported to be oncogenic in various malignancies. However, the role and mechanism of linc01133 in regulating gastric cancer growth is still not clear. In the present study, we found that linc01133 was significantly up-regulated in gastric cancer tissues compared to non-tumorous gastric tissues. Linc01133 over-expression significantly correlated with tumor size and tumor differentiation in gastric cancer patients. The expression of linc01133 was regulated by c-Jun and c-Fos collaboratively. In both in vitro and in vivo studies, linc01133 was shown to promote gastric cancer cell growth. Linc01133 localized in the cytoplasm and functioned as an endogenous competing RNA of miR-145-5p to up-regulate the expression of YES1，which was proved to be the target gene of miR-145-5p. By promoting YES1-dependent YAP1 nuclear translocation, linc01133 up-regulated the expression of the key cell cycle regulators CDK4, CDK6 and cyclin D1 to promote G1-S phase transition. Thus, our study unveiled the function and mechanism of linc01133 regulating cell cycle progression in gastric cancer.

2021-12-21 | GSE191227 | GEO

Gene expression in pancreatic ductal adenocarcinoma

Project description:To further develop our understanding of the gene expression signature of pancreatic ductal adenocarcinoma Gene expression signatures in macrodissected resected pancreatic ductal adenocarcinoma specimens

2014-03-14 | E-GEOD-55643 | biostudies-arrayexpress

SAMD1 suppresses epithelial-mesenchymal transition pathways in pancreatic ductal adenocarcinoma [ChIP-Seq]

Project description:SAMD1 suppresses epithelial-mesenchymal transition pathways in pancreatic ductal adenocarcinoma [ChIP-Seq]

| PRJNA999242 | ENA

SAMD1 suppresses epithelial-mesenchymal transition pathways in pancreatic ductal adenocarcinoma [RNA-Seq]

Project description:SAMD1 suppresses epithelial-mesenchymal transition pathways in pancreatic ductal adenocarcinoma [RNA-Seq]

| PRJNA999243 | ENA

Expression profiling of pancreatic adenocarcinoma and ductal adenocarcinoma cell lines.

Project description:We characterized baseline gene expression profiles for eleven human pancreatic adenocarcinoma and ductal adenocarcinoma cell lines.

2018-11-22 | GSE122818 | GEO

MS-based proteomic analysis of pancreatic ductal adenocarcinoma

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2022-03-21 | PXD032681 | JPOST Repository

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