ArticleMolecular medicine reports2019
Downregulation of LINC01638 lncRNA inhibits migration and invasion of pancreatic ductal adenocarcinoma cells by reducing TGF‑β signaling.
Article in Molecular medicine reports, 2019. 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, 11 citations in OpenAlex.
- Functional, Pharmacogenomic, and Immune Landscapes of Long Non-Coding RNAs in Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Interplay between TGF-β signaling and long non-coding RNAs in digestive system cancers: mechanisms and biological implications.Human cell · 2025Review
- The Past, Present, and Future of Biomarkers for the Early Diagnosis of Pancreatic Cancer.Biomedicines · 2024Review
- Plasma-derived exosomal long noncoding RNAs of pancreatic cancer patients as novel blood-based biomarkers of disease.BMC cancer · 2024Article
- LINC01638 sustains human mesenchymal stem cell self-renewal and competency for osteogenic cell fate.Scientific reports · 2023Article
- ETS like-1 protein ELK1-induced lncRNA LINC01638 accelerates the progression of papillary thyroid cancer by regulating Axin2 through Wnt/β-catenin signaling pathway.Bioengineered · 2021Article
- Biomarkers in the diagnosis of pancreatic cancer: Are we closer to finding the golden ticket?World journal of gastroenterology · 2021Review
- Non-coding RNAs in pancreatic ductal adenocarcinoma: New approaches for better diagnosis and therapy.Translational oncology · 2021Review
- Article
- Regulation of Hippo, TGFβ/SMAD, Wnt/Frontiers in oncology · 2021Review
- Research progress on long non-coding RNAs and their roles as potential biomarkers for diagnosis and prognosis in pancreatic cancer.Cancer cell international · 2020Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
LINC01638 is a long non‑coding RNA (lncRNA) with an oncogenic role in breast cancer, while its involvement in other malignancies is unknown. This study was performed to investigate the potential role of LINC01638 in pancreatic ductal adenocarcinoma (PDAC). The expression of LINC01638 was determined via reverse transcription‑quantitative polymerase chain reaction analysis, whereas the levels of transforming growth factor‑β1 (TGF‑β1) in plasma were measured via ELISA. Receiver operating characteristic curve analysis was conducted to determine the diagnostic value of LINC01638. Additionally, the migratory and invasive abilities of cells were evaluated via Transwell migration and invasion assays. In the present study, LINC01638 was significantly upregulated in tumor tissues compared with adjacent healthy tissues in the majority of patients with PDAC. Plasma levels of LINC01638 were significantly higher in patients with PDAC compared with in healthy controls. In effect, upregulation of plasma LINC01638 distinguished patients with PDAC from healthy controls in receiver operating characteristic analysis. Plasma levels of LINC01638 and TGF‑β1 were positively correlated in patients with PDAC, but not in healthy controls. LINC01638 overexpression increased TGF‑β1 expression, while silencing of LINC01638 using short hairpin RNA (shRNA) led to reduced TGF‑β1 expression in a PDAC cell line. LINC01638 overexpression promoted, while shRNA silencing inhibited, migration and invasion of cell of a PDAC cell line. Treatment with exogenous TGF‑β1 attenuated the inhibitory effect of LINC01638 shRNA silencing on cancer cell migration and invasion. It is concluded that LINC01638 lncRNA may be involved in the migration and invasion of PDAC cells via regulation of TGF‑β1.
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