Abstract
We investigated the role of LINC00312 in pancreatic cancer (PC) and its underlying mechanism. LINC00312 levels were assessed in PC tissues and cell lines using qRT-PCR, and its correlation with clinical indicators was analyzed. Overexpression and knockdown models of LINC00312 were created in PC cell lines. The effects of LINC00312 on PC cell function were evaluated through CCK-8 and Transwell migration assays, and the binding between LINC00312 and the downstream target gene FGD4 was examined using a dual luciferase reporter gene assay. LINC00312 levels were significantly lower in PC tissues compared to adjacent tissues. High LINC00312 levels were associated with increased incidence of lymphatic and distant metastasis. PC cell lines exhibited downregulated LINC00312 expression. LINC00312 overexpression reduced cell proliferation and migration, while knockdown had the opposite effect. Bioinformatics analysis and luciferase reporter assays confirmed that LINC00312 binds to FGD4. Western blot analysis revealed reduced FGD4 levels upon LINC00312 overexpression, and a negative correlation between FGD4 and LINC00312 expression in PC. Moreover, FGD4 promoted PC cell proliferation and migration, its overexpression counteracted the inhibitory effects of LINC00312 overexpression on PC progression. Downregulation of LINC00312 in PC tissues and cell lines. LINC00312 overexpression suppresses PC cell proliferation and migration by negatively regulating FGD4. Thus, LINC00312 represents a potential therapeutic target for PC.
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