Open AccessLong non‐coding RNA HOTAIR/microRNA‐206 sponge regulates STC2 and further influences cell biological functions in head and neck squamous cell carcinoma
Author(s) -
Li Tiancheng,
Qin Yao,
Zhen Zhen,
Shen Hong,
Cong Tiechuan,
Schiferle Erik,
Xiao Shuifang
Publication year - 2019
Publication title -
cell proliferation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.647
H-Index - 74
eISSN - 1365-2184
pISSN - 0960-7722
DOI - 10.1111/cpr.12651
Subject(s) - hotair , head and neck squamous cell carcinoma , cancer research , microrna , biology , cell growth , long non coding rna , downregulation and upregulation , protein kinase b , pi3k/akt/mtor pathway , hox gene , signal transduction , microbiology and biotechnology , gene expression , gene , cancer , genetics , head and neck cancer
Objective It is essential to characterize underlying molecular mechanism associated with head and neck squamous cell carcinoma (HNSCC) and identify promising therapeutic targets. Herein, we explored role of homeobox transcript antisense RNA (HOTAIR) in HNSCC to regulate stanniocalcin‐2 (STC2) by sponging microRNA‐206 (miR‐206). Methods HNSCC‐related differentially expressed genes and regulation network amongst HOTAIR, miR‐206 and STC2 were identified. Next, effect of HOTAIR on cell biological functions of HNSCC was identified after transfection of cells with HOTAIR overexpressed plasmids or siRNA against HOTAIR. PI3K/AKT signalling pathway‐related gene expression was measured after miR‐206 and STC2 were suppressed. Cell invasion, migration and proliferation were assessed. Finally, tumour growth was assessed to determine the effects of HOTAIR/miR‐206/STC2 axis in vivo. Results HOTAIR specifically bound to miR‐206 and miR‐206 targeted STC2. Downregulated HOTAIR or upregulated miR‐206 suppressed HNSCC cell proliferation, invasion and migration. miR‐206 inhibited PI3K/AKT signalling pathway by down‐regulating STC2. Besides, silenced HOTAIR or overexpressed miR‐206 repressed the tumour growth of nude mice with HNSCC. Conclusion HOTAIR regulated HNSCC cell biological functions by binding to miR‐206 through STC2.