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CCHE1 accelerated the initiation of oral squamous cell carcinoma through enhancing PAK2 expression by sponging miR‐922
Author(s) -
Wang Yongliang,
Tong Junjie,
Lin Haozhi,
Ma Lei,
Xu Yaoxiang
Publication year - 2020
Publication title -
journal of oral pathology and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.887
H-Index - 83
eISSN - 1600-0714
pISSN - 0904-2512
DOI - 10.1111/jop.12995
Subject(s) - gene knockdown , flow cytometry , cancer research , cell growth , oncogene , apoptosis , downregulation and upregulation , biology , cell , microrna , cell culture , microbiology and biotechnology , gene , cell cycle , biochemistry , genetics
Background Oral squamous cell carcinoma (OSCC) is a normal form of mouth cancer, comprising the majority of oral cancers. A large number of long non‐coding RNAs (lncRNAs) have been reported due to their oncogenic function in cancers. Recent studies show that lncRNA CCHE1 is an oncogene in a wide range of cancers. Whether CCHE1 accelerates the progression of OSCC is still undiscovered. Methods The qRT‐PCR analysis was used to determine CCHE1, miR‐922, and PAK2 expression levels. CCK8 and colony formation assays were applied to evaluate OSCC cell proliferative ability. Transwell assay was performed to investigate the capability of cell migration and invasion. Cell apoptosis was assessed by flow cytometry analysis. The distribution of CCHE1 in OSCC cells was confirmed via subcellular fractionation assay. Luciferase reporter assay was used to verify the connection between miR‐922 and CCHE1 or PAK2. Results qRT‐PCR analysis identified the upregulation of CCHE1 in OSCC cells. Knockdown of CCHE1 curbed the proliferation, migration, and invasion and hastened the apoptosis in OSCC cell lines. Moreover, it was found that miR‐922 could interact with CCHE1. Besides, PAK2 was identified as the target gene of miR‐922 and its expression was negatively modulated by miR‐922 and positively regulated by CCHE1. Restoration assay manifested that the suppressing influence of CCHE1 depletion on OSCC progression was rescued by amplified PAK2. Conclusions CCHE1 increases the expression of PAK2 to promote the progression of OSCC by competitively binding to miR‐922 in OSCC cells.