Regulatory mechanism of lncRNA HCP5 in nasopharyngeal carcinoma cell proliferation and apoptosis via the miR-140-5p/NPR3 axis

Objectives Nasopharyngeal carcinoma (NPC) is malignant tumor frequently occurring in east and southeast Asia. This study investigated the underlying mechanism of lncRNA HCP5 in NPC cell proliferation and apoptosis. Methods LncRNA HCP5 expression in NPC cells and tissues was detected. SUNE-1 cells were transfected with HCP5 silencing and CNE-1 cells were transfected with overexpressing HCP5, and then cell proliferation and apoptosis were measured. Subcellular localization of HCP5 was analyzed. The binding relationship between lncRNA HCP5 and miR-140-5p, and miR-140-5p and NPR3 were predicted and verified. Expressions of miR-140-5p and NPR3 in NPC cells were detected. SUNE-1 cells and CNE-1 cells were transfected with miR-140-5p mimic, and si-HCP5-transfected SUNE-1 cells were treated with miR-140-5p inhibitor. Then the proliferation and apoptosis of NPC cells were detected. Results LncRNA HCP5 was elevated in NPC tissues and cells. HCP5 silencing suppressed NPC cell proliferation and enhanced apoptosis. HCP5 was mainly located in the cytoplasm of NPC cells. HCP5 promoted NPR3 expression by competitively binding to miR-140-5p. Overexpression of miR-140-5p weakened proliferation and facilitated apoptosis of NPC cells. miR-140-5p inhibitor partially restored the effects of HCP5 silencing on NPC cells. Conclusion LncRNA HCP5 upregulated NPR3 expression via sponging miR-140-5p, thereby suppressing NPC cell proliferation and promoting apoptosis. This study may offer new insights into NPC treatment.