ArticleEpigenetics2011
Aberrant TGFβ/SMAD4 signaling contributes to epigenetic silencing of a putative tumor suppressor, RunX1T1 in ovarian cancer.
Article in Epigenetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 43 citations in OpenAlex.
- Smad4 restricts injury-provoked biliary proliferation and carcinogenesis.Disease models & mechanisms · 2024Article
- Article
- Prediction of Chemoresistance-How Preclinical Data Could Help to Modify Therapeutic Strategy in High-Grade Serous Ovarian Cancer.Current oncology (Toronto, Ont.) · 2023Review
- Review
- Comparing the Secretomes of Chemorefractory and Chemoresistant Ovarian Cancer Cell Populations.Cancers · 2022Review
- Exploration of the underlying biological differences and targets in ovarian cancer patients with diverse immunotherapy response.Frontiers in immunology · 2022Article
- RUNX1T1, a potential prognostic marker in breast cancer, is co-ordinately expressed with ERα, and regulated by estrogen receptor signalling in breast cancer cells.Molecular biology reports · 2021Article
- Importance of Potential New Biomarkers in Patient with Serouse Ovarian Cancer.Diagnostics (Basel, Switzerland) · 2021Article
- Cyproheptadine, an epigenetic modifier, exhibits anti-tumor activity by reversing the epigenetic silencing of IRF6 in urothelial carcinoma.Cancer cell international · 2021Article
- Epigenetic Silencing of STAT3-Targeted miR-193a, by Constitutive Activation of JAK/STAT Signaling, Leads to Tumor Progression Through Overexpression of YWHAZ in Gastric Cancer.Frontiers in oncology · 2021Article
- Environmental Factor-Mediated Transgenerational Inheritance ofFrontiers in immunology · 2020Article
- E2F6 functions as a competing endogenous RNA, and transcriptional repressor, to promote ovarian cancer stemness.Cancer science · 2019Article
- Epigenetic Biomarkers in the Management of Ovarian Cancer: Current Prospectives.Frontiers in cell and developmental biology · 2019Review
- Integrated genomic characterization of cancer genes in glioma.Cancer cell international · 2017Article
- C/EBPβ regulates homeostatic and oncogenic gastric cell proliferation.Journal of molecular medicine (Berlin, Germany) · 2016Article
- NEpiC: a network-assisted algorithm for epigenetic studies using mean and variance combined signals.Nucleic acids research · 2016Article
- Aberrant JAK/STAT Signaling Suppresses TFF1 and TFF2 through Epigenetic Silencing of GATA6 in Gastric Cancer.International journal of molecular sciences · 2016Article
- Epigenetic silencing of the NR4A3 tumor suppressor, by aberrant JAK/STAT signaling, predicts prognosis in gastric cancer.Scientific reports · 2016Article
- BCAT1 expression associates with ovarian cancer progression: possible implications in altered disease metabolism.Oncotarget · 2015Article
- Global transcriptomic analysis of model human cell lines exposed to surface-modified gold nanoparticles: the effect of surface chemistry.Nanoscale · 2015Article
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Authors and funding
18 authors at 8 institutions in 2 countries.
Funding
Abstract
Aberrant TGFβ signaling pathway may alter the expression of down-stream targets and promotes ovarian carcinogenesis. However, the mechanism of this impairment is not fully understood. Our previous study has identified RunX1T1 as a putative SMAD4 target in an immortalized ovarian surface epithelial cell line, IOSE. In this study, we report that transcription of RunX1T1 was confirmed to be positively regulated by SMAD4 in IOSE cells and epigenetically silenced in a panel of ovarian cancer cell lines by promoter hypermethylation and histone methylation at H3 lysine 9. SMAD4 depletion increased repressive histone modifications of RunX1T1 promoter without affecting promoter methylation in IOSE cells. Epigenetic treatment can restore RunX1T1 expression by reversing its epigenetic status in MCP3 ovarian cancer cells. When transiently treated with a demethylating agent, the expression of RunX1T1 was partially restored in MCP3 cells, but gradual re-silencing through promoter re-methylation was observed after the treatment. Interestingly, SMAD4 knockdown accelerated this re-silencing process, suggesting that normal TGF-beta signaling is essential for the maintenance of RunX1T1 expression. In vivo analysis confirmed that hypermethylation of RunX1T1 was detected in 35.7% (34/95) of ovarian tumors with high clinical stages (P=0.035) and in 83% (5/6) of primary ovarian cancer-initiating cells. Additionally, concurrent methylation of RunX1T1 and another SMAD4 target, FBXO32 which was previously found to be hypermethylated in ovarian cancer was observed in this same sample cohort (P< 0.05). Restoration of RunX1T1 inhibited cancer cell growth. Taken together, dysregulated TGFβ/SMAD4 signaling may lead to epigenetic silencing of a putative tumor suppressor, RunX1T1, during ovarian carcinogenesis.
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