Background: Oral squamous cell carcinoma (OSCC) is the predominant histological type of human oral cancer. In this study, we sought to investigate the functional role of lncRNA HCP5 in OSCC progression.
Methods: The HCP5 and miR-140-5p expression level was determined in 73 paired OSCC tissues and their adjacent normal tissues. Knockdown or overexpression of HCP5 was conducted to investigate the effects of HCP5 on malignant behaviors of OSCC cells. Then, bioinformatic prediction and dual-luciferase reporter assay were conducted to study the interaction between HCP5 and miR-140-5p in OSCC.
Results: Our results demonstrated that HCP5 expression was significantly increased in OSCC tissues and cell lines. High HCP5 level was associated with the aggressive clinicopathological characteristics and poor prognosis of OSCC patients. In vitro gain- and loss-of-function experiments showed that HCP5 overexpression promoted, whereas HCP5 knockdown inhibited the proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) of OSCC cells. Mechanistically, we confirmed that HCP5 might serve as a competitive endogenous RNA (ceRNA) for miR-140-5p to alleviate the repression of its downstream target, SOX4, a master regulator of EMT. Furthermore, restoration of miR-140-5p expression diminished the oncogenic effects of HCP5 on OSCC cells.
Conclusion: Overall, the present study indicated that HCP5/miR-140-5p/SOX4 axis might be a ponderable and promising therapeutic target for OSCC.
Keywords: oral squamous cell carcinoma, long non-coding RNA HCP5, epithelial-mesenchymal transition, competitive endogenous RNA