Yongliang Wang1, Junjie Tong2, Haozhi Lin2, Lei Ma1, Yaoxiang Xu2,3. 1. Department of Prosthodontics, The Affiliated Hospital of Qingdao University, Qingdao, China. 2. Department of Oral Medicine, The Affiliated Hospital of Qingdao University, Qingdao, China. 3. Dental Digital Medicine & 3D Printing Engineering Laboratory of Qingdao University, Qingdao, China.
Abstract
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.
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.