ArticleMolecular and cellular biology1999
All-trans-retinoic acid inhibits Jun N-terminal kinase by increasing dual-specificity phosphatase activity.
Article in Molecular and cellular biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 95 citations in OpenAlex.
- Retinoic acid signaling and metabolism in heart failure.American journal of physiology. Heart and circulatory physiology · 2025Review
- Transcription networks in liver development and acute liver failure.Liver research (Beijing, China) · 2023Review
- Mead acid inhibits retinol-induced irritant contact dermatitis via peroxisome proliferator-activated receptor alpha.Frontiers in molecular biosciences · 2023Article
- Antitumor Effects of a New Retinoate of the Fungal Cytotoxin Illudin M in Brain Tumor Models.International journal of molecular sciences · 2022Article
- All-Trans Retinoic Acid Attenuates Blue Light-Induced Apoptosis of Retinal Photoreceptors by Upregulating MKP-1 Expression.Molecular neurobiology · 2021Article
- Synergistic Antiproliferative Effects of All-Trans Retinoic Acid and Paclitaxel on Autosomal Dominant Polycystic Kidney Disease Epithelial Cells.BioMed research international · 2021Article
- Methyl viologen induces neural differentiation on murine P19 cells.In vitro cellular & developmental biology. Animal · 2016Article
- Article
- Transcriptional and posttranslational regulation of insulin-like growth factor binding protein-3 by Akt3.Carcinogenesis · 2014Article
- Retinoic acid-elicited RARα/RXRα signaling attenuates Aβ production by directly inhibiting γ-secretase-mediated cleavage of amyloid precursor protein.ACS chemical neuroscience · 2013Article
- 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
- Combined α-tocopherol and ascorbic acid protects against smoke-induced lung squamous metaplasia in ferrets.Lung cancer (Amsterdam, Netherlands) · 2012Article
- Animal models in carotenoids research and lung cancer prevention.Translational oncology · 2011Article
- The role of retinoic acid in tolerance and immunity.Immunity · 2011Review
- Retinoic acid treatment of human leiomyoma cells transformed the cell phenotype to one strongly resembling myometrial cells.Clinical endocrinology · 2008Article
- Kinase-dependent, retinoic acid receptor-independent up-regulation of cyclooxygenase-2 by all-trans retinoic acid in human mesangial cells.British journal of pharmacology · 2006Article
- Article
- Regulation of ERK1 gene expression by coactivator proteins.The Biochemical journal · 2005Article
- Retinoic acid and arsenic trioxide cooperate for apoptosis through phosphorylated RXR alpha.Oncogene · 2005Article
- 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
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Jun N-terminal kinases (JNKs) are serine-threonine kinases that play a critical role in the regulation of cell growth and differentiation. We previously observed that JNK activity is suppressed by all-trans-retinoic acid (t-RA), a ligand for retinoic acid nuclear receptors (RARs), in normal human bronchial epithelial cells, which are growth inhibited by t-RA. In this study, we investigated the mechanism by which t-RA inhibits JNK and the possibility that this signaling event is blocked in non-small cell lung cancer (NSCLC) cells. Virtually all NSCLC cell lines are resistant to the growth-inhibitory effects of t-RA, and a subset of them have a transcriptional defect specific to retinoid nuclear receptors. We found that in NSCLC cells expressing functional retinoid receptors, serum-induced JNK phosphorylation and activity were inhibited by t-RA in a bimodal pattern, transiently within 30 min and in a sustained fashion beginning at 12 h. Retinoid receptor transcriptional activation was required for the late, but not the early, suppression of JNK activity. t-RA inhibited serum-induced JNK activity by blocking mitogen-activated protein (MAP) kinase kinase 4-induced signaling events. This effect of t-RA was phosphatase dependent and involved an increase in the expression of the dual-specificity MAP kinase phosphatase 1 (MKP-1). t-RA did not activate MKP-1 expression or inhibit JNK activity in a NSCLC cell line with retinoid receptors that are refractory to ligand-induced transcriptional activation. These findings provide the first evidence that t-RA suppresses JNK activity by inhibiting JNK phosphorylation. Retinoid receptor transcriptional activation was necessary for the sustained inhibition of JNK activity by t-RA, and this signaling event was disrupted in NSCLC cells with retinoid receptors that are refractory to ligand-induced transcriptional activation.
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