ArticleOncogene2005
Cellular retinol-binding protein-I inhibits PI3K/Akt signaling through a retinoic acid receptor-dependent mechanism that regulates p85-p110 heterodimerization.
Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
28 citing papers in PubMed, 54 citations in OpenAlex.
- Article
- Anoikis resistance of small airway epithelium is involved in the progression of chronic obstructive pulmonary disease.Frontiers in immunology · 2023Article
- Altered RBP1 Gene Expression Impacts Epithelial Cell Retinoic Acid, Proliferation, and Microenvironment.Cells · 2022Article
- Methylation-Mediated Silencing ofJournal of oncology · 2022Article
- Cellular retinol binding protein 1 transfection reduces proliferation and AKT-related gene expression in H460 non-small lung cancer cells.Molecular biology reports · 2020Article
- C-SH2 point mutation converts p85β regulatory subunit of phosphoinositide 3-kinase to an anti-aging gene.Scientific reports · 2019Article
- Role of retinoids in the prevention and treatment of colorectal cancer.World journal of gastrointestinal oncology · 2015Review
- Vitamin A, cancer treatment and prevention: the new role of cellular retinol binding proteins.BioMed research international · 2015Review
- Long-acting progestin-only contraceptives enhance human endometrial stromal cell expressed neuronal pentraxin-1 and reactive oxygen species to promote endothelial cell apoptosis.The Journal of clinical endocrinology and metabolism · 2014Article
- Identification of host-immune response protein candidates in the sera of human oral squamous cell carcinoma patients.PloS one · 2014Article
- Activation of Akt pathway by transcription-independent mechanisms of retinoic acid promotes survival and invasion in lung cancer cells.Molecular cancer · 2013Article
- A heterozygous IDH1R132H/WT mutation induces genome-wide alterations in DNA methylation.Genome research · 2012Article
- Reversal by RARα agonist Am580 of c-Myc-induced imbalance in RARα/RARγ expression during MMTV-Myc tumorigenesis.Breast cancer research : BCR · 2012Article
- Prenatal retinoic acid upregulates pulmonary gene expression of PI3K and AKT in nitrofen-induced pulmonary hypoplasia.Pediatric surgery international · 2010Article
- Interference with Sin3 function induces epigenetic reprogramming and differentiation in breast cancer cells.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Identification of a CpG island methylator phenotype that defines a distinct subgroup of glioma.Cancer cell · 2010Article
- Spatiotemporal alteration in phosphatidylinositide 3-kinase-serine/threonine protein kinase B signaling in the nitrofen-induced hypoplastic lung.Journal of pediatric surgery · 2010Article
- Article
- A genome-wide association study in 574 schizophrenia trios using DNA pooling.Molecular psychiatry · 2009Article
- Activation of the PI3 kinase pathway by retinoic acid mediates sodium/iodide symporter induction and iodide transport in MCF-7 breast cancer cells.Cancer research · 2009Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Downregulation of the cellular retinol-binding protein-I (CRBP-I) occurs in breast and other human cancers, but its significance is not well understood. Recently, we showed that restoration of CRBP-I expression in transformed MTSV1-7 breast epithelial cells increased retinoic receptor activity, inhibited anoikis, promoted acinar differentiation and inhibited tumorigenicity, suggesting that CRBP-I suppresses tumor progression. However, the mechanism underlying these effects of CRBP-I was not elucidated. Here we demonstrate, using genetic and pharmacological approaches, that CRBP-I inhibits, in a retinoic acid receptor-dependent manner, the PI3K/Akt survival pathway. Inhibition of PI3K/Akt was necessary and sufficient to explain the antitumor effects of CRBP-I and was mediated by decreased p85 regulatory and p110 catalytic subunit heterodimerization. We present evidence consistent with the idea that this effect is due to CRBP-I inhibition of p85 phosphorylation at Y688. To our knowledge, this is the first demonstration of PI3K regulation at the level of p85-p110 heterodimerization. These findings lead us to hypothesize that CRBP-I downregulation in cancer promotes tumor progression through inhibition of retinoic acid receptor activity and derepression of PI3K/Akt signaling via a novel mechanism.
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Registered trials
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.