scholarly journals Modulation of retinoic acid sensitivity in lung cancer cells through dynamic balance of orphan receptors nur77 and COUP-TF and their heterodimerization

1997 ◽  
Vol 16 (7) ◽  
pp. 1656-1669 ◽  
Author(s):  
Q. Wu
Keyword(s):  
Lung Cancer ◽  
Retinoic Acid ◽  
Cancer Cells ◽  
Dynamic Balance ◽  
Lung Cancer Cells ◽  
Orphan Receptors ◽  
Acid Sensitivity

miR-29b and retinoic acid co-delivery: a promising tool to induce a synergistic antitumoral effect in non-small cell lung cancer cells

2020 ◽  
Vol 10 (5) ◽  
pp. 1367-1380 ◽  
Author(s):  
Mariana Magalhães ◽  
Joana Jorge ◽  
Ana Cristina Gonçalves ◽  
Ana Bela Sarmento-Ribeiro ◽  
Rui Carvalho ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Retinoic Acid ◽  
Small Cell Lung Cancer ◽  
Cancer Cells ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Lung Cancer Cells ◽  
Small Cell Lung ◽  
Antitumoral Effect ◽  
Promising Tool

Retinoic acid down-regulates VPAC1 receptors and TGF-β3 but up-regulates TGF-β2 in lung cancer cells

Peptides ◽  
2000 ◽  
Vol 21 (12) ◽  
pp. 1831-1837 ◽  
Author(s):  
Sonia B Jakowlew ◽  
Halina Zakowicz ◽  
Terry W Moody
Keyword(s):  
Lung Cancer ◽  
Retinoic Acid ◽  
Cancer Cells ◽  
Lung Cancer Cells

scholarly journals c-Jun N-Terminal Kinase Contributes to Aberrant Retinoid Signaling in Lung Cancer Cells by Phosphorylating and Inducing Proteasomal Degradation of Retinoic Acid Receptor α

2005 ◽  
Vol 25 (3) ◽  
pp. 1054-1069 ◽  
Author(s):  
Harish Srinivas ◽  
Denise M. Juroske ◽  
Shailaja Kalyankrishna ◽  
Dianna D. Cody ◽  
Roger E. Price ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Retinoic Acid ◽  
Cancer Cells ◽  
Retinoic Acid Receptor ◽  
Cancer Cell Line ◽  
Lung Cancer Cell Line ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Retinoid Signaling ◽  
Phosphopeptide Mapping

ABSTRACT Retinoic acid (RA) is the ligand for nuclear RA receptors (RARs and RXRs) and is crucial for normal epithelial cell growth and differentiation. During malignant transformation, human bronchial epithelial cells acquire a block in retinoid signaling caused in part by a transcriptional defect in RARs. Here, we show that activation of c-Jun N-terminal kinase (JNK) contributes to RAR dysfunction by phosphorylating RARα and inducing degradation through the ubiquitin-proteasomal pathway. Analysis of RARα mutants and phosphopeptide mapping revealed that RARα residues Thr181, Ser445, and Ser461 are phosphorylated by JNK. Mutation of these residues to alanines prevented efficient ubiquitination of RARα and increased the stability of the protein. We investigated the importance of RARα phosphorylation by JNK as a mediator of retinoid resistance in lung cancer. Mice that develop lung cancer from activation of a latent K-ras oncogene had high intratumoral JNK activity and low RARα levels and were resistant to treatment with an RAR ligand. JNK inhibition in a human lung cancer cell line enhanced RARα levels, ligand-induced activity of RXR-RAR dimers, and growth inhibition by RA. These findings point to JNK as a key mediator of aberrant retinoid signaling in lung cancer cells.

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