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

GSE267702 Homo sapiens Expression profiling by high throughput sequencing 6 samples Submitted 2024/07/17 Platform GPL23227
Summary
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.
Published in
LINC01133 promotes pancreatic ductal adenocarcinoma epithelial-mesenchymal transition mediated by SPP1 through binding to Arp3
Yang Y, Gong Y, Ding Y et al. · Cell death & disease 2024 · PMID 38987572 · doi:10.1038/s41419-024-06876-3
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Also filed as BioProject PRJNA1112428 and SRA study SRP508196. Searching any of these in the dataset finder brings you back here.

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