TET1 inhibits the migration and invasion of cervical cancer cells by regulating autophagy
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ABSTRACT:
PROVIDER: PRJNA990741 | ENA |
REPOSITORIES: ENA
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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.
2024-03-13 | GSE236315 | GEO
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.
2024-03-13 | GSE236396 | GEO
Project description:TET1 inhibits the migration and invasion of cervical cancer cells by regulating autophagy [RNA-seq]
| PRJNA990751 | ENA
Project description:TET1 inhibits the migration and invasion of cervical cancer cells by regulating autophagy [MeDIP-Seq]
| PRJNA989659 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below.
2024-03-13 | GSE236397 | GEO
Project description:Ten-Eleven Translocation 1 (TET1) is a member of methylcytosine dioxygenase, which catalyse 5-methylcytosine (5-mC) to 5-hydroxymethylcytosine (5-hmC) that promote the demethylation process. The diminished expression of TET1 protein and 5-hmC in many tumors indicate a critical role for the maintenance of cell stability. However, role of TET1 in bladder cancer development remains unclear. Here we found that TET1 expression was downregulated in bladder cancer tissues compared with normal urothelium and was inversely related to patient overall survival. TET1 silencing in bladder cancer cells increase proliferation and inhibited cell migration and invasion while its re-expression inhibits their proliferation and the growth of tumor xenografts. Furthermore, we found that TET1 binds to the promoter of the TSG to maintain its hypomethylated which interacts with β-catenin and suppress its nuclear translocation, thus inhibiting β-catenin transcriptional activity and downstream genes. In conclusion, TET1 acts as a tumor suppressor gene in bladder cancer cells by suppressing β-catenin signaling. This study may facilitate efforts to therapeutic strategy for patients with bladder cancer.
2020-06-16 | GSE137646 | GEO
Project description:Circular RNA (circRNA) is newly type of noncoding RNA that are formed by back-splicing of exon and play the important functions in tumorigenesis. However, the research of circRNA is deficient in cervical cancer (CC). We performed high-throughput sequencing on cervical cancer tissues and normal cervical control samples. We discovered the up-regulated circYPEL2 (has_circ_0005400) in cervical cancer and used this as a potential research object through bioinformatics analysis. Finally, through RNA sequencing and bioinformatics technology, we analyzed the downstream targeted genes that may be affected by circYPEL2.
2022-01-31 | GSE173112 | GEO
Project description:During adult neurogenesis, newly formed olfactory bulb (OB) interneurons migrate radially to integrate into specific layers of the OB. Despite the importance of this process, the intracellular mechanisms that regulate radial migration remain poorly understood. Here we find that microRNA (miRNA) let-7 regulates radial migration by modulating autophagy in new-born neurons. Using Argonaute2-immunoprecipitation, we performed global profiling of miRNAs in adult-born OB neurons and identified let-7 as a highly abundant miRNA family. Knockdown of let-7 in migrating neuroblasts prevented radial migration and led to an immature morphology of newly formed interneurons. This phenotype was accompanied by a decrease in autophagic activity. Overexpression of Beclin-1 or TFEB in new-born neurons lacking let-7 resulted in re-activation of autophagy and restored radial migration. Thus, these results reveal a miRNA-dependent link between autophagy and adult neurogenesis with implications for neurodegenerative diseases where these processes are impaired.
2017-03-28 | GSE83903 | GEO
Project description:Background:Ten-eleven translocation (TET) enzymes catalyze the oxidation of 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC) promoting demethylation in cells. However, the expression pattern and biologic significance of TET in papillary thyroid carcinoma (PTC) remain unclear. This study aimed to elucidate the biological functions of TET1 and the miRNA and mRNA expression levels in PTC cells with downregulated TET1. Methods:The expression of the TET family in 49 PTC tissues and corresponding tumor-adjacent tissues, as well as PTC cell lines (BCPAP, K1, and TPC-1) and the normal thyroid epithelial cell line (Nthy-ori 3-1), were detected using quantitative real-time polymerase chain reaction. The 5hmC level was detected in PTC tissues and cell lines using immunohistochemistry and dot blot assay, respectively. After silencing the TET1 gene with siRNAs in BCPAP and TPC-1?cells, cell proliferation was detected using EdU assay. Transwell assay was used to investigate cell migration and invasion. miRNA and mRNA expression arrays were conducted in TET1-depleted BCPAP cells. Results:The expression level of TET1 decreased in PTC tissues and cell lines and was consistent with the reduction in the 5hmC level. The knockdown of the TET1 gene with siRNAs in BCPAP and TPC-1?cells, cell proliferation was detected using EdU assay. Transwell assay was used to investigate cell migration and invasion. miRNA and mRNA expression arrays were conducted in TET1-depleted BCPAP cells. WNT4, FZD4, CDK6, MCF2L, and EDN1 was upregulated as potential target genes of dysregulated miRNAs. Conclusion:The study showed that TET1 dysfunction inhibited the migration and invasion of BCPAP cells and might have a potential role in the pathogenesis of PTC.
| S-EPMC7031722 | biostudies-literature
Project description:The potential risk of P2Y12 antagonists for cancer treatment is controversial. Here we show that PSB 0739, a P2Y12 antagonist inhibits human cervical cancer cells (Hela and SiHa) migration without modifying cell proliferation. We identify that the co-acetylation and lactylation of epithelial-mesenchymal transition (EMT)-related protein NCL, MYH9, CTTN, S100A6, and ALDOA revealed by proteomic analysis of posttranslational modifications (PTM), are responsible for the PSB0739-induced migration inhibition in human cervical cancer cells. Our data suggest that as one of P2Y12 antagonists, PSB 0739 has no risk in cervical cancer cell migration. The co-modification of acetylation and lactylation of EMT-associated proteins would be novel promising targets to develop new drug for cancer cell migration beyond contributing the potential mechanism of the use of PSB0379 in human cervical cancer cells.
2023-04-06 | PXD041371 |