Background: LINC01503 has been reported to act as a candidate oncogenic lncRNA in several types of human cancer. However, the functions and underlying mechanisms of LINC01503 in gastric cardia adenocarcinoma (GCA) remain unclear.
Aims: To investigate the roles and underlying mechanisms of LINC01503 in GCA progression.
Materials and methods: Gene expressions were detected by quantitative real-time PCR (qRT-PCR). Gain-of-function assays were performed to evaluate the function of LINC01503 in gastric cancer cells. Bioinformatics analysis, luciferase reporter assay, and RIP assay were performed to identify associations among LINC01503, miR-133a-5p, and VIM.
Results: The expression level of LINC01503 was significantly elevated in GCA tissues and cell lines. High expression of LINC01503 was correlated with lymph node metastasis, TNM stage, and poor prognosis of GCA patients. Knockdown of LINC01503 significantly reduced proliferation, migration, and invasion ability in GC cells. LINC01503 might function as a competing endogenous RNA (ceRNA) via sponging miR-133a-5p to upregulate the expression of VIM. Furthermore, overexpression of LINC01503 promoted the progression of epithelial mesenchymal transition (EMT) in vitro.
Conclusion: LINC01503 serves as an oncogenic lncRNA to promote GCA progression via affecting LINC01503/miR-133a-5p/VIM axis and EMT process. LINC01503 not only has a critical role in GCA progression but also provide a novel potential biomarker in predicting prognosis for GCA patients.
Keywords: Epithelial mesenchymal transition; Gastric cardia adenocarcinoma; LINC01503; VIM; miR-133a-5p.
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