LINC01133 promotes pancreatic ductal adenocarcinoma epithelial-mesenchymal transition mediated by SPP1 through binding to Arp3.
Yefan YangYuxi GongYing DingShuning SunRumeng BaiShuaishuai ZhuoZhi-Hong ZhangPublished in: Cell death & disease (2024)
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.
Keyphrases
- long non coding rna
- poor prognosis
- epithelial mesenchymal transition
- long noncoding rna
- end stage renal disease
- cell proliferation
- newly diagnosed
- chronic kidney disease
- ejection fraction
- signaling pathway
- peritoneal dialysis
- binding protein
- transforming growth factor
- genome wide
- risk assessment
- single cell
- gene expression
- dna methylation
- genome wide identification
- patient reported
- cell cycle arrest