ArticleMedical oncology (Northwood, London, England)2006
Growth inhibition and differentiation induced by peroxisome proliferator activated receptor gamma ligand rosiglitazone in human melanoma cell line A375.
Article in Medical oncology (Northwood, London, England), 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 41 citations in OpenAlex.
- PPAR-γ in Melanoma and Immune Cells: Insights into Disease Pathogenesis and Therapeutic Implications.Cells · 2025Review
- Molecular Characterization of Cancer Preventive and Therapeutic Potential of Three Antistress Compounds, Triethylene Glycol, Withanone, and Withaferin A.International journal of molecular sciences · 2025Article
- Role of Ciminalum-4-thiazolidinone Hybrids in Molecular NF-κB Dependent Pathways.International journal of molecular sciences · 2024Article
- PPARs and the Kynurenine Pathway in Melanoma-Potential Biological Interactions.International journal of molecular sciences · 2023Review
- The role of peroxisome proliferator-activated receptors in the tumor microenvironment, tumor cell metabolism, and anticancer therapy.Frontiers in pharmacology · 2023Review
- Bexarotene inhibits cell proliferation by inducing oxidative stress, DNA damage and apoptosis via PPARγ/ NF-κB signaling pathway in C6 glioma cells.Medical oncology (Northwood, London, England) · 2021Article
- PPAR-γ Modulators as Current and Potential Cancer Treatments.Frontiers in oncology · 2021Review
- Accelerated Barrier Repair in Human Skin Explants Induced with a Plant-Derived PPAR-α Activating Complex via Cooperative Interactions.Clinical, cosmetic and investigational dermatology · 2021Article
- Cloxiquine, a traditional antituberculosis agent, suppresses the growth and metastasis of melanoma cells through activation of PPARγ.Cell death & disease · 2019Article
- Bexarotene inhibits the viability of non-small cell lung cancer cells via slc10a2/PPARγ/PTEN/mTOR signaling pathway.BMC cancer · 2018Article
- Nuclear receptor function in skin health and disease: therapeutic opportunities in the orphan and adopted receptor classes.Cellular and molecular life sciences : CMLS · 2016Review
- Chemotherapy and chemoprevention by thiazolidinediones.BioMed research international · 2015Review
- Nuclear hormone receptor functions in keratinocyte and melanocyte homeostasis, epidermal carcinogenesis and melanomagenesis.FEBS letters · 2013Review
- Coffee component hydroxyl hydroquinone (HHQ) as a putative ligand for PPAR gamma and implications in breast cancer.BMC genomics · 2013Article
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- Peroxisome proliferator-activated receptors (PPARs) in dermatology: Challenge and promise.Dermato-endocrinology · 2011Article
- PPARalpha/gamma expression and activity in mouse and human melanocytes and melanoma cells.Pharmaceutical research · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLigands of peroxisome proliferator-activated receptors (PPARs) have been demonstrated to be antitumorgenic in vitro and in vivo due to their antiproliferative, prodifferential, and antiangiogenic effects. The aim of this study is to evaluate the effects and mechanisms of PPARgamma ligand rosiglitazone (ROZ) on the growth, apoptosis, and differentiation in human melanoma cancer cell line A375.
methodsThe effects of ROZ on A375 cell proliferation were measured by clonogenic assay, apoptosis and cell cycle kinetics by FACS with ROZ for 72 h, PPARgamma protein was detected by Western blot analysis and immunocytochemical staining, and PPARgamma mRNA expression by RT-PCR. The differentiation effect of ROZ was determined by measurement of melanin content and tyrosinase activity. The levels of Bcl-2, P53, p-ERK, and ERK were also detected by Western blot analysis. Inhibition of tumorigensis was observed in nude mice.
resultsROZ inhibited colony formation and induced apoptosis in A375 cells, and the cells were arrested in G1 phase. This effect was associated with a decrease of the expression of Bcl-2 and increase of the expression of P53. ROZ also induced the differentiation in A375 cells. ROZ increased expression of PPARgamma and decreased the expression of ERK and p-ERK. Data in vivo showed that ROZ could inhibit tumorigensis in nude mice.
conclusionThese results demonstrated that ROZ inhibited growth of A375 cells via the induction of apoptosis, necrosis, and differentiation in a PPARgamma-dependent manner and might present a promising therapeutic approach in certain human maligancies.
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