Helenalin-mediated post-transcriptional regulation of p21(Cip1) inhibits 3T3-L1 preadipocyte proliferation.

Journal of Cellular Biochemistry
Karishma M FernandesRon F Morrison

Abstract

We have previously shown that post-transcriptional mechanisms involving the 26S proteasome regulate the cyclin-dependent kinase inhibitors (CKIs), p21(Cip1) and p27(Kip1) during preadipocyte proliferation. Earlier studies further demonstrated that the anti-inflammatory, anti-carcinogenic phytochemical, helenalin is a potent inhibitor of periodic Skp2 accumulation, an F-box protein mediating SCF E3 ligase ubiquitylation and degradation of both CKIs during S phase progression. Data presented here demonstrate that helenalin dose-dependently induced G1 arrest of synchronously replicating 3T3-L1 preadipocytes. This effect occurred in the absence of discernable indices of cell toxicity or apoptosis under the conditions used in this study. Our results demonstrate that helenalin markedly increased p21 protein accumulation in both density-arrested and proliferating preadipocytes in a dose-dependent manner. This increase in p21 protein abundance occurred without change in mRNA transcript demonstrating that post-transcriptional mechanisms were involved. This notion was further supported by the modest accumulation of polyubiquitylated p21 following treatment with helenalin suggesting that suppression of targeted p21 proteolysis by the 26S ...Continue Reading

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Aug 28, 2009·International Journal of Cancer. Journal International Du Cancer·Ali NaderiIan C Bennett
Jun 5, 2018·Evidence-based Complementary and Alternative Medicine : ECAM·María Laura GonzálezMaría Cecilia Carpinella
Feb 16, 2011·Natural Product Reports·Andrea Vasas, Judit Hohmann
Jul 3, 2020·Recent Patents on Anti-cancer Drug Discovery·Priyanka Kriplani, Kumar Guarve

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