ArticleCell death & disease2024
LINC01133 promotes pancreatic ductal adenocarcinoma epithelial-mesenchymal transition mediated by SPP1 through binding to Arp3.
Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Targeting lncRNA-regulated macrophage polarization: a novel therapeutic strategy for pancreatic ductal adenocarcinoma.Journal of physiology and biochemistry · 2026Review
- m6A Modification-Mediated LINC01547 Promotes Pancreatic Cancer Growth and Gemcitabine Resistance Through miR-34a-5p/MYH9 Axis.Biochemical genetics · 2026Article
- Spatial Location of SPP1Cancer science · 2026Article
- SPP1+ Macrophages and the Orchestration of Spatially Organized Immunosuppression in Cancer.Biomedicines · 2026Review
- Metastasis-Specific Biomarker SPP1 and its Characterization in Colorectal Cancer with HIV Infection.Current HIV research · 2026Article
- Scar-associated macrophages and biliary epithelial cells interaction exacerbates hepatic fibrosis in biliary atresia.Pediatric research · 2026Article
- SPP1 regulates tumor progression through modulation of signaling pathways and the tumor microenvironment.Discover oncology · 2025Review
- The Good, the Bad, or Both? Unveiling the Molecular Functions of LINC01133 in Tumors.Non-coding RNA · 2025Article
- Application of non‑coding RNAs in tumors (Review).Molecular medicine reports · 2025Review
- Lymphocyte antigen 6 family member E suppresses apoptosis and promotes pancreatic cancer growth and migration via Wnt/β-catenin pathway activation.Scientific reports · 2024Article
- Osteopontin in pancreatic cancer: A systematic review.Medicine internationalArticle
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Authors and funding
7 authors.
Funding
Abstract
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.
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