ArticleMolecular and cellular biology1995
Evidence for impaired retinoic acid receptor-thyroid hormone receptor AF-2 cofactor activity in human lung cancer.
Article in Molecular and cellular biology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.
- Association between Retinoic acid receptor-β hypermethylation and NSCLC risk: a meta-analysis and literature review.Oncotarget · 2017Pooled it
- MiR-30a and miR-379 modulate retinoic acid pathway by targeting DNA methyltransferase 3B in oral cancer.Journal of biomedical science · 2020Article
- Why Differentiation Therapy Sometimes Fails: Molecular Mechanisms of Resistance to Retinoids.International journal of molecular sciences · 2018Review
- RARβ2 hypermethylation is associated with poor recurrence-free survival in never-smokers with adenocarcinoma of the lung.Clinical epigenetics · 2015Article
- Molecular pathways: current role and future directions of the retinoic acid pathway in cancer prevention and treatment.Clinical cancer research : an official journal of the American Association for Cancer Research · 2013Review
- Akt phosphorylates and suppresses the transactivation of retinoic acid receptor alpha.The Biochemical journal · 2006Article
- c-Jun N-terminal kinase contributes to aberrant retinoid signaling in lung cancer cells by phosphorylating and inducing proteasomal degradation of retinoic acid receptor alpha.Molecular and cellular biology · 2005Article
- Review
- WNT7a induces E-cadherin in lung cancer cells.Proceedings of the National Academy of Sciences of the United States of America · 2003Article
- Article
- Orphan receptor COUP-TF is required for induction of retinoic acid receptor beta, growth inhibition, and apoptosis by retinoic acid in cancer cells.Molecular and cellular biology · 2000Article
- All-trans-retinoic acid inhibits Jun N-terminal kinase by increasing dual-specificity phosphatase activity.Molecular and cellular biology · 1999Article
- Integration of growth factor, extracellular matrix, and retinoid signals during bronchial epithelial cell differentiation.Molecular and cellular biology · 1998Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Retinoic acid (RA) is required for normal airway epithelial cell growth and differentiation both in vivo and in vitro. One of the earliest events following the exposure of bronchial epithelial cells to RA is the strong induction of RA receptor beta (RAR beta) mRNA. Previous work established that many lung cancer cell lines and primary tumors display abnormal RAR beta mRNA expression, most often absence or weak expression of the RAR beta 2 isoform, even after RA treatment. Restoration of RAR beta 2 into RAR beta-negative lung cancer cell lines has been reported to inhibit tumorigenicity. Since RAR beta 2 inactivation may contribute to lung cancer, we have investigated the molecular mechanism of defective RAR beta 2 expression. Nuclear run-on assays and transient transfections with RAR beta 2 promoter constructs indicate the presence of trans-acting transcriptional defects in most lung cancer cell lines, which map to the RA response element (RARE). These defects cannot be complemented by RAR-retinoid X receptor cotransfection and can be separated into two types: (i) one affecting transcription from direct repeat RAREs, but not palindromic RAREs, and (ii) another affecting transcription from both types of RARE. Studies using chimeras between RAR alpha, TR alpha, and other transcription factors suggest the existence of novel RAR-thyroid hormone receptor AF-2-specific cofactors, which are necessary for high levels of transcription. Furthermore, these factors may be frequently inactivated in human lung cancer.
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