TET1 inhibits the migration and invasion of cervical cancer cells by regulating autophagy
Ji Ren,
Xiuying Chen,
Jing Li,
Yuxin Zan,
Shan Wang,
Yujie Tan,
Yan Ding
Affiliations
Ji Ren
Hubei Key Laboratory of Embryonic Stem Cell Research, Taihe Hospital, Hubei Provincial Clinical Research Center for Umbilical Cord Blood Hematopoietic Stem Cells, Hubei University of Medicine, Shiyan, Hubei, China
Xiuying Chen
Hubei Key Laboratory of Embryonic Stem Cell Research, Taihe Hospital, Hubei Provincial Clinical Research Center for Umbilical Cord Blood Hematopoietic Stem Cells, Hubei University of Medicine, Shiyan, Hubei, China
Jing Li
Gynecology, Wuhan Children’s Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
Yuxin Zan
Hubei Key Laboratory of Embryonic Stem Cell Research, Taihe Hospital, Hubei Provincial Clinical Research Center for Umbilical Cord Blood Hematopoietic Stem Cells, Hubei University of Medicine, Shiyan, Hubei, China
Shan Wang
Hubei Key Laboratory of Embryonic Stem Cell Research, Taihe Hospital, Hubei Provincial Clinical Research Center for Umbilical Cord Blood Hematopoietic Stem Cells, Hubei University of Medicine, Shiyan, Hubei, China
Yujie Tan
Center for Clinical Laboratories, the Affiliated Hospital of Guizhou Medical University, Guiyang, China
Yan Ding
Hubei Key Laboratory of Embryonic Stem Cell Research, Taihe Hospital, Hubei Provincial Clinical Research Center for Umbilical Cord Blood Hematopoietic Stem Cells, Hubei University of Medicine, Shiyan, Hubei, China
Methylation modifications play pertinent roles in regulating gene expression and various biological processes. The silencing of the demethylase enzyme TET1 can affect the expressions of key oncogenes or tumour suppressor genes, thus contributing to tumour formation. Nonetheless, how TET1 affects the progression of cervical cancer is yet to be elucidated. In this study, we found that the expression of TET1 was significantly downregulated in cervical cancer tissues. Functionally, TET1 knockdown in cervical cancer cells can promote cell proliferation, migration, invasion, cervical xenograft tumour formation and EMT. On the contrary, its overexpression can reverse the aforementioned processes. Moreover, the autophagy level of cervical cancer cells can be enhanced after TET1 knockdown. Mechanistically, methylated DNA immunoprecipitation (MeDIP)-sequencing and MeDIP quantitative real-time PCR revealed that TET1 mediates the methylation of autophagy promoter regions. These findings suggest that TET1 affects the autophagy of cervical cancer cells by altering the methylation levels of NKRF or HIST1H2AK, but the specific mechanism needs to be investigated further.
