Yajing Zhou1, Hua Chai2, Lei Guo3, Zhongqiu Dai3, Jianming Lai4, Jianping Duan3, Yanting Liu5, Qian Ding3. 1. Department of Physical Therapy, Qingdao No.6 People's Hospital, Qingdao, Shandong, People's Republic of China. 2. Department of Liver Disease, Qingdao No.6 People's Hospital, Qingdao, Shandong, People's Republic of China. 3. Department of Infectious Diseases, Qingdao No.6 People's Hospital, Qingdao, Shandong, People's Republic of China. 4. Medical College, 12593Qingdao University, Qingdao, Shandong, People's Republic of China. 5. Department of Ten Areas of Liver Disease, Qingdao No.6 People's Hospital, Qingdao, Shandong, People's Republic of China.
Abstract
AIM: This study aimed to evaluate the effects of centromere protein W (CENPW, also known as CUG2) in hepatocellular carcinoma (HCC). METHODS: CENPW expression in HCC tissues and cells was detected by RT-qPCR assay. CCK-8 and colony formation assay were used to assess cell proliferation. Wound healing and Transwell assay was used to detect cell migration and invasion, respectively. The flow cytometry was used to analyze the cell cycle distribution and apoptosis. RESULTS: CENPW expression was upregulated in HCC tissues and cells. Knockdown of CENPW inhibited cell proliferation, migration, and invasion and induced the G0/G1 phase arrest and cell apoptosis in HCC cells, which might involve the E2F signaling regulation. CONCLUSION: CENPW acted as an oncogenic role in HCC progression via activation E2F signaling. Our findings may provide new insights into the studying mechanisms of HCC.
AIM: This study aimed to evaluate the effects of centromere protein W (CENPW, also known as CUG2) in hepatocellular carcinoma (HCC). METHODS:CENPW expression in HCC tissues and cells was detected by RT-qPCR assay. CCK-8 and colony formation assay were used to assess cell proliferation. Wound healing and Transwell assay was used to detect cell migration and invasion, respectively. The flow cytometry was used to analyze the cell cycle distribution and apoptosis. RESULTS:CENPW expression was upregulated in HCC tissues and cells. Knockdown of CENPW inhibited cell proliferation, migration, and invasion and induced the G0/G1 phase arrest and cell apoptosis in HCC cells, which might involve the E2F signaling regulation. CONCLUSION:CENPW acted as an oncogenic role in HCC progression via activation E2F signaling. Our findings may provide new insights into the studying mechanisms of HCC.
Entities:
Keywords:
CENPW (also known as CUG2); E2F signaling; cell cycle; cell proliferation; hepatocellular carcinoma