ArticleThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology2016
p53 signaling is involved in leptin-induced growth of hepatic and breast cancer cells.
Article in The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- Role of ubiquitin-specific proteases in programmed cell death of breast cancer cells.Genes & diseases · 2025Review
- Targeting the deubiquitinaseOncology reports · 2023Review
- Cathepsin B maturation plays a critical role in leptin-induced hepatic cancer cell growth through activation of NLRP3 inflammasomes.Archives of pharmacal research · 2023Article
- USP2-Related Cellular Signaling and Consequent Pathophysiological Outcomes.International journal of molecular sciences · 2021Review
- The Adipokine Component in the Molecular Regulation of Cancer Cell Survival, Proliferation and Metastasis.Pathology oncology research : POR · 2021Review
- FOXN4 Inhibits Breast Cancer Progression By Direct Activation Of P53.OncoTargets and therapy · 2020Article
- Article
- Obesity and Breast Cancer: Role of Leptin.Frontiers in oncology · 2019Review
- Leptin regulation of the p53-HIF1α/PKM2-aromatase axis in breast adipose stromal cells: a novel mechanism for the obesity-breast cancer link.International journal of obesity (2005) · 2018Article
- The Molecular Mechanisms of Regulation on USP2's Alternative Splicing and the Significance of Its Products.International journal of biological sciences · 2017Review
- Apoptotic Impact of Heliox Cold Plasma on a Cervical Cell Line Using Gold Nanoparticle-Doped Graphene Oxide Nanosheets.Iranian journal of pharmaceutical research : IJPRArticle
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
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Abstract
Leptin, an adipokine predominantly produced from adipose tissue, is well known to induce tumor growth. However, underlying molecular mechanisms are not established yet. While p53 has long been well recognized as a potent tumor suppressor gene, accumulating evidence has also indicated its potential role in growth and survival of cancer cells depending on experimental environments. In the present study, we examined if p53 signaling is implicated in leptin-induced growth of cancer cells. Herein, we demonstrated that leptin treatment significantly increased p53 protein expression in both hepatic (HepG2) and breast (MCF-7) cancer cells without significant effect on mRNA expression. Enhanced p53 expression by leptin was mediated via modulation of ubiquitination, in particular ubiquitin specific protease 2 (USP2)-dependent manner. Furthermore, gene silencing of p53 by small interfering RNA (siRNA) suppressed leptin-induced growth of hepatic and breast cancer cells, indicating the role of p53 signaling in tumor growth by leptin. In addition, we also showed that knockdown of p53 restored suppression of caspase-3 activity by leptin through modulating Bax expression and prevented leptin-induced cell cycle progression, implying the involvement of p53 signaling in the regulation of both apoptosis and cell cycle progression in cancer cells treated with leptin. Taken together, the results in the present study demonstrated the potential role of p53 signaling in leptin-induced tumor growth.
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