ArticleCell death & disease2019
TBL1 is required for the mesenchymal phenotype of transformed breast cancer cells.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- Targeting the DNA damage response through TBL1X in mantle cell lymphoma.Blood advances · 2025Article
- PPM1G-mediated TBL1X mRNA splicing promotes cell migration in hepatocellular carcinoma.Cancer science · 2025Article
- EP300 promotes tumor stemness via epigenetic activation of CRISP3 leading to lobaplatin resistance in triple-negative breast cancer.Human cell · 2024Article
- Comparing the roles of sex chromosome-encoded protein homologs in gene regulation.Genes & development · 2024Review
- Article
- Research progress of Claudin-low breast cancer.Frontiers in oncology · 2023Review
- TBL1X: At the crossroads of transcriptional and posttranscriptional regulation.Experimental hematology · 2022Review
- ARID1A downregulation promotes cell proliferation and migration of colon cancer via VIM activation and CDH1 suppression.Journal of cellular and molecular medicine · 2022Article
- Two lncRNAs, MACC1-AS1 and UCA1, co-mediate the expression of multiple mRNAs through interaction with individual miRNAs in breast cancer cells.Non-coding RNA research · 2022Article
- TBL1X and Flot2 form a positive feedback loop to promote metastasis in nasopharyngeal carcinoma.International journal of biological sciences · 2022Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The epithelial-to-mesenchymal transition (EMT) and its reversion (MET) are related to tumor cell dissemination and migration, tumor circulating cell generation, cancer stem cells, chemoresistance, and metastasis formation. To identify chromatin and epigenetic factors possibly involved in the process of EMT, we compare the levels of expression of epigenetic genes in a transformed human breast epithelial cell line (HMEC-RAS) versus a stable clone of the same cell line expressing the EMT master regulator ZEB1 (HMEC-RAS-ZEB1). One of the factors strongly induced in the HMEC-RAS-ZEB1 cells was Transducin beta-like 1 (TBL1), a component of the NCoR complex, which has both corepressor and coactivator activities. We show that TBL1 interacts with ZEB1 and that both factors cooperate to repress the promoter of the epithelial gene E-cadherin (CDH1) and to autoactivate the ZEB1 promoter. Consistent with its central role, TBL1 is required for mesenchymal phenotypes of transformed breast epithelial and breast cancer cell lines of the claudin-low subtype. Importantly, a high expression of the TBL1 gene correlates with poor prognosis and increased proportion of metastasis in breast cancer patients, indicating that the level of TBL1 expression can be used as a prognostic marker.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.