Yujing Wang1, Jing Wang2, Chunmei Liu3, Min Li4. 1. Department of Clinical Laboratory, Qilu Hospital (Qingdao), Cheeloo College of Medicine, Shandong University, Qingdao, China, 1597965013@qq.com. 2. Qingdao Municipal Hospital, Qingdao, China. 3. Qingdao Research and Development Center of Lanzhou Institute of Chemical Physics, Chinese Academy of Sciences, Qingdao, China. 4. Department of Gynecology, Qilu Hospital of Shandong University, Jinan, China.
Abstract
OBJECTIVE: Silent information regulator 1 (SIRT1), an NAD+-dependent III class histone deacetylase, plays crucial roles in cell proliferation, apoptosis, senescence, metabolism, and stress responses. Nevertheless, the role of SIRT1 in tumorigenesis remains unclear. METHODS: In the present study, we measured expression levels of SIRT1 and HPV16 E7 protein in cervical cancer (CC) tissue and calculated their correlations. We measured the effect of silencing SIRT1 on the proliferation, migration, invasion, and apoptosis in human CC SiHa cells. RESULTS: Immunohistochemistry results revealed that the expression of SIRT1 was upregulated with progression from CIN II-III to CC, but was not expressed in normal cervical tissues and CIN I. There was a positive correlation between SIRT1 expression and HPV16 E7 expression in CC tissues, and silencing of HPV16 E7 downregulated the expression of SIRT1. Depletion of SIRT1 downregulated SIRT1 expression, and inhibited proliferation, migration, and invasion of SiHa cells, inducing apoptosis. CONCLUSIONS: Taken together, the data suggest that SIRT1 promotes CC carcinogenesis. SIRT1 inhibition is a potential treatment strategy for CC.
OBJECTIVE: Silent information regulator 1 (SIRT1), an NAD+-dependent III class histone deacetylase, plays crucial roles in cell proliferation, apoptosis, senescence, metabolism, and stress responses. Nevertheless, the role of SIRT1 in tumorigenesis remains unclear. METHODS: In the present study, we measured expression levels of SIRT1 and HPV16 E7 protein in cervical cancer (CC) tissue and calculated their correlations. We measured the effect of silencing SIRT1 on the proliferation, migration, invasion, and apoptosis in human CC SiHa cells. RESULTS: Immunohistochemistry results revealed that the expression of SIRT1 was upregulated with progression from CIN II-III to CC, but was not expressed in normal cervical tissues and CIN I. There was a positive correlation between SIRT1 expression and HPV16 E7 expression in CC tissues, and silencing of HPV16 E7 downregulated the expression of SIRT1. Depletion of SIRT1 downregulated SIRT1 expression, and inhibited proliferation, migration, and invasion of SiHa cells, inducing apoptosis. CONCLUSIONS: Taken together, the data suggest that SIRT1 promotes CC carcinogenesis. SIRT1 inhibition is a potential treatment strategy for CC.