Project description:Two cervicitis and four cervical squamous cell carcinoma (two I-IIa and two IIb-IV) were selected from the medical records of the Department of Gynecology of Yuhuangding Hospital from January to July 2017. These six samples were performed MeDIP and hMeDIP-seq to characterize the global pattern of 5mC and 5hmC.
Project description:Methylation modifications play pertinent roles in regulating gene expression and various biological processes. The silencing of the demethylated modifier TET1 can affect the expressions of key oncogenes or tumor suppressor genes, thus contributing to tumor 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 tumor 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 malignant biological behavior of cervical cancer cells by altering the methylation levels of autophagy genes NKRF and HIST1H2AK, but the specific mechanism needs to be investigated further.
Project description:Utilizing methylation DNA immunoprecipitation (MeDIP) coupled with promoter tiling arrays, we analyzed the methylation profiles of pooled DNA from human cervical carcinoma and normal cervix
Project description:Utilizing methylation DNA immunoprecipitation (MeDIP) coupled with promoter tiling arrays, we analyzed the methylation profiles of pooled DNA from human cervical carcinoma and normal cervix Cervical carcinoma compaire with normal cervix
Project description:Methylation modifications play pertinent roles in regulating gene expression and various biological processes. The silencing of the demethylated modifier TET1 can affect the expressions of key oncogenes or tumor suppressor genes, thus contributing to tumor 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 tumor 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 malignant biological behavior of cervical cancer cells by altering the methylation levels of autophagy genes NKRF and HIST1H2AK, but the specific mechanism needs to be investigated further.
Project description:we used methylated DNA immunoprecipitation sequencing (MeDIP-Seq) to detect DNA methylation levels and lncRNA-seq to detect lncRNA expression levels in 3 lung cancer samples and 3 matched normal samples. Then 255 differentially methylated genes (DMGs) and 246 differentially expressed lncRNAs (DELs) were identified. Finally, LINC01354 was founded to be differentially methylated and predictive of transcription. Besides, the prognostic value of differential methylation related DELs was analyzed.