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Down‐regulation of lncRNA HCG11 promotes cell proliferation of oral squamous cell carcinoma through sponging miR‐455‐5p
Author(s) -
Wu Jingjing,
Li Yong,
Liu Jian,
Xu Yanzhi
Publication year - 2021
Publication title -
the journal of gene medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.689
H-Index - 91
eISSN - 1521-2254
pISSN - 1099-498X
DOI - 10.1002/jgm.3293
Subject(s) - cell growth , gene knockdown , cancer research , cell cycle , flow cytometry , cell , biology , chemistry , cell culture , microbiology and biotechnology , genetics
Abstract Background As a type of head and neck squamous cell carcinoma (HNSCC), oral squamous cell carcinoma (OSCC) has a high incidence and low survival rate. Frequent deletion of protein tyrosine phosphatase receptor type sigma (PTPRS) has been found in HNSCC. Long non‐coding RNA (lncRNA) HCG11 and miR‐455‐5p have been reported to be involved in several cancers, in which miR‐455‐5p was found to be up‐regulated in the OSCC. However, the role of HCG11 in OSCC development is still unclear. Methods Several co‐transfection systems were established to explore the regulation of HCG11 on OSCC cells. Cell proliferation was evaluated by the MTT assay, flow cytometry of cell cycle distribution, immunofluorescence of Ki67 and western blotting. A dual luciferase reporter assay was performed to verify the binding effects of miR‐455‐5p on HCG11 and PTPRS. The role of HCG11 knockdown in OSCC cell growth was also confirmed by nude mouse tumorigenicity assay in vivo . Results Knockdown of HCG11 increased OSCC cell proliferation, as indicated by enhanced cell vitalities over time, increased G1/S transition and Ki67 levels. Furthermore, lncRNA HCG11 was shown to negatively regulate miR‐455‐5p and miR‐455‐5p targeted PTPRS directly to affect its downstream indicators, which can further modulate OSCC cell proliferation and growth. The results obtained in vivo confirmed that HCG11 knockdown promoted OSCC cell growth. Conclusions The lncRNA HCG11/miR‐R‐455‐5p axis can be considered as an upstream signalling circuit of PTPRS with respect to regulating its activity and downstream pathways to further influence the progression of OSCC. This finding may provide a novel RNA‐based therapeutic target for OSCC treatment.