LncRNA HCP5 promotes the progression of gastric cancer through the miR-526b/PBX3 axis.

Abstract

Objectives: To investigate whether LncRNA HLA complex P5 (HCP5) promotes gastric cancer (GC) via the miR-526b/Pre-B Cell Leukemia Homeobox 3 (PBX3) pathway.

Methods: Thirteen paired GC and adjacent non-tumorous tissues, along with NCI-N87 GC cells, were analyzed. HCP5 expression levels were measured, and its impact on cell viability, proliferation, and migration were evaluated. Dual-luciferase reporter assays were performed to confirm the direct interactions among HCP5, miR-526b, and PBX3. The effects of HCP5 overexpression or silencing on miR-526b and PBX3 expression were analyzed. A miR-526b mimic was transfected for functional rescue.

Results: HCP5 was significantly upregulated, while miR-526b was downregulated in GC tissues. Dual-luciferase assays confirmed the direct binding of HCP5 to miR-526b and of miR-526b to PBX3. In NCI-N87 cells, HCP5 overexpression downregulated miR-526b and upregulated PBX3 expression, whereas silencing HCP5 showed the opposite effects. Moreover, HCP5 overexpression decreased Bax and increased Bcl-2 levels, which was reversed by miR-526b mimic transfection. Functionally, HCP5 enhanced GC cell viability and migration, both of which were suppressed by miR-526b. HCP5 promoted cell proliferation, as evidenced by a reduced proportion of cells in the G0/G1 phase, which was reversed by miR-526b.

Conclusions: HCP5 acts as an oncogenic lncRNA in GC by promoting cell viability, migration, and proliferation via the miR-526b/PBX3 axis. Targeting the HCP5/miR-526b/PBX3 axis may represent a promising therapeutic strategy for GC.