Targeting to the non-genomic activity of retinoic acid receptor-gamma by acacetin in hepatocellular carcinoma View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2017-12

AUTHORS

Wenjun Zeng, Chunyun Zhang, Hongwei Cheng, Yun-Long Wu, Jie Liu, Zekun Chen, Jian-gang Huang, Russell Erick Ericksen, Liqun Chen, Haiping Zhang, Alice Sze Tsai Wong, Xiao-kun Zhang, Weiping Han, Jin-Zhang Zeng

ABSTRACT

We recently demonstrated that retinoic acid receptor-γ (RARγ) is overexpressed and acts as a tumor promoter in hepatocellular carcinoma (HCC). The oncogenic activity of RARγ is mainly attributed to its physiological interaction with p85α regulatory subunit of PI3K leading to constitutive activation of AKT. Here we report RARγ as a negative regulator of p53 signaling and thus extend the oncogenic potential of RARγ to a new role in controlling the balance between AKT and p53. A natural flavonoid acacetin is then identified to be capable of modulating RARγ-dependent AKT-p53 network. It specifically binds to RARγ and inhibits all-trans retinoic acid (atRA) stimulation of RARγ transactivation. However, the anticancer action of acacetin is independent on its modulation of RARγ-driven transcriptional activity. Acacetin induces cancer cell apoptosis through antagonizing the non-genomic effect of RARγ on AKT and p53. When bound to RARγ, acacetin prevents RARγ from its activation of AKT followed by recovery of the normal p53 signaling. Given the implication of AKT-p53 dysregulation in most HCC, targeting the non-genomic signaling of RARγ that switches AKT-p53 from a pro-survival to a pro-apoptotic program in cancer cells should be a promising strategy for developing novel anti-HCC drugs. More... »

PAGES

348

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/s41598-017-00233-5

DOI

http://dx.doi.org/10.1038/s41598-017-00233-5

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1084130369

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/28336971


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