Kaifeng Qiu1, Zixian Huang2, Zhiquan Huang3, Zhichao He4, Siping You4. 1. Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou 510120, China; Department of Pharmacy, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, Guangdong, China; Department of Pharmacy, Zengcheng People's Hospital (Boji-affiliated Hospital of Sun Yat-sen University), Guangzhou, Guangdong, China. 2. Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou 510120, China; Department of Oral and Maxillofacial Surgery, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, Guangdong 510120, China. 3. Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou 510120, China; Department of Oral and Maxillofacial Surgery, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, Guangdong 510120, China. Electronic address: zhiquanhuang1978@126.com. 4. Department of Pharmacy, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, Guangdong, China.
Abstract
OBJECTIVES: Tongue squamous cell carcinoma (TSCC) is the most common type of head and neck squamous cell carcinoma (HNSCC) in China, and its survival rate remains unsatisfactory. miR-22 has been identified as a tumor suppressor in many human cancers, and high expression of CD147 occurs in many tumors. The aim of the present study was to investigate the expression and function of miR-22 in TSCC and its relationship with the expression of CD147. METHODS: TCA8113 cells were transiently transfected with a miR-22 mimic/inhibitor. Subsequently, a validation with Real-time RT-PCR was performed to analyze the miR-22 expression level, and a CCK-8 proliferation assay and transwell migration and invasion assays were carried out. Cotransfections using As-miR-22/si-CD147 mRNA or a miR-22/CD147 overexpression vector were applied, and we investigated the biological effects on cotranscribed TCA8113 cells. RESULTS: qRT-PCR confirmed that miR-22 or As-miR-22 were successfully transfected into TCA8113 cells. Suppressing miR-22 resulted in a promotion of cell proliferation and motility and an up-regulation of CD147 in TCA8113 cells in vitro. In contrast, increasing miR-22 inhibited cell proliferation and motility and down-regulated CD147. Furthermore, the reduction or overexpression of CD147 can reverse the promoting or suppressive effects of miR-22, respectively. CONCLUSIONS: The down-expression of miR-22 can regulate cell growth and motility in TSCC cells, which indicates that miR-22 acts as a tumor suppressor in TSCC. Additionally, CD147 is subsequently up-regulated when miR-22 inhibited. Taken together, the findings of this research defined a novel relationship between the down-regulation of miR-22 and the up-regulation of CD147 and demonstrated that CD147 is a downstream factor of miR-22.
OBJECTIVES:Tongue squamous cell carcinoma (TSCC) is the most common type of head and neck squamous cell carcinoma (HNSCC) in China, and its survival rate remains unsatisfactory. miR-22 has been identified as a tumor suppressor in many humancancers, and high expression of CD147 occurs in many tumors. The aim of the present study was to investigate the expression and function of miR-22 in TSCC and its relationship with the expression of CD147. METHODS: TCA8113 cells were transiently transfected with a miR-22 mimic/inhibitor. Subsequently, a validation with Real-time RT-PCR was performed to analyze the miR-22 expression level, and a CCK-8 proliferation assay and transwell migration and invasion assays were carried out. Cotransfections using As-miR-22/si-CD147 mRNA or a miR-22/CD147 overexpression vector were applied, and we investigated the biological effects on cotranscribed TCA8113 cells. RESULTS: qRT-PCR confirmed that miR-22 or As-miR-22 were successfully transfected into TCA8113 cells. Suppressing miR-22 resulted in a promotion of cell proliferation and motility and an up-regulation of CD147 in TCA8113 cells in vitro. In contrast, increasing miR-22 inhibited cell proliferation and motility and down-regulated CD147. Furthermore, the reduction or overexpression of CD147 can reverse the promoting or suppressive effects of miR-22, respectively. CONCLUSIONS: The down-expression of miR-22 can regulate cell growth and motility in TSCC cells, which indicates that miR-22 acts as a tumor suppressor in TSCC. Additionally, CD147 is subsequently up-regulated when miR-22 inhibited. Taken together, the findings of this research defined a novel relationship between the down-regulation of miR-22 and the up-regulation of CD147 and demonstrated that CD147 is a downstream factor of miR-22.