Abstract Background Long non-coding RNA PVT1 (lncRNA PVT1) serves as a carcinogenic regulatory factor in several cancers; however, the expre
Abstract Background Long non-coding RNA PVT1 (lncRNA PVT1) serves as a carcinogenic regulatory factor in several cancers; however, the expression and function of its transcriptional isomer PVT1-214 in gastric cancer (GC) are poorly understood. Methods PVT1-214 and miR-671-5p levels in GC cells and tissues were analyzed through quantitative real-time polymerase chain reaction (qRT-PCR). Western blotting (WB) was used to detect Homo sapiens solute carrier family 45 member 4 (SLC45A4) expression in GC cells. Thereafter, the relationship between PVT1-214 and miR-671-5p was evaluated through dual-luciferase reporter assays and RNA immunoprecipitation (RIP) analysis. Additionally, the biological activities of PVT1-214, miR-671-5p and SLC45A4 in GC cells were analyzed through Cell Counting Kit-8 (CCK-8), 5-ethyl-20-deoxyuridine (EdU), colony formation and Transwell assays. The effect of PVT1-214 on GC was studied in vivo via a nude mouse tumor xenograft model. Results PVT1-214 overexpression in GC cells and tissues was positively related to tumor size, malignancy grade, lymphatic metastasis and clinical stage. PVT1-214 knockdown suppressed cell growth, invasion and migration in vitro, whereas PVT1-214 overexpression promoted tumor proliferation in vivo. In addition, PVT1-214 positively regulates SLC45A4 expression through its competitive endogenous RNA (ceRNA) activity against miR-671-5p. SLC45A4 expression was positively related to PVT1-214 expression. PVT1-214 competes with endogenous RNA (ceRNA) by binding to miR-671-5p. When miR-671-5p is inhibited, SLC45A4 is released from the complementary binding complex, thereby increasing SLC45A4 protein levels in GC cells. Conclusions The present work revealed the candidate ceRNA regulatory pathway by which PVT1-214 regulates SLC45A4 expression in GC cells, which is achieved through competitive binding to endogenous miR-671-5p. The results of this study can shed novel light on new molecular targets for treating GC.
