ArticleJournal of cellular and molecular medicine2019
Pristimerin attenuates cell proliferation of uveal melanoma cells by inhibiting insulin-like growth factor-1 receptor and its downstream pathways.
Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 20 citations in OpenAlex.
- Research Progress of Natural Compounds from Chinese Herbal Medicine in the Treatment of Melanoma.Current treatment options in oncology · 2025Review
- Pristimerin Exerts Pharmacological Effects Through Multiple Signaling Pathways: A Comprehensive Review.Drug design, development and therapy · 2024Review
- New insights into the prognosis of intraocular malignancy: Interventions for association mechanisms between cancer and diabetes.Frontiers in oncology · 2022Review
- Skin anomalies in acromegalic patients (Review of the practical aspects).Experimental and therapeutic medicine · 2021Review
- Review
- Cellular and Molecular Mechanisms of Pristimerin in Cancer Therapy: Recent Advances.Frontiers in oncology · 2021Review
- Article
- Pristimerin Suppresses RANKL-Induced Osteoclastogenesis and Ameliorates Ovariectomy-Induced Bone Loss.Frontiers in pharmacology · 2020Article
- Pristimerin attenuates cell proliferation of uveal melanoma cells by inhibiting insulin-like growth factor-1 receptor and its downstream pathways.Journal of cellular and molecular medicine · 2019Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Uveal melanoma (UM) has a high mortality rate due to liver metastasis. The insulin-like growth factor-1 receptor (IGF-1R) is highly expressed in UM and has been shown to be associated with hepatic metastases. Targeting IGF signalling may be considered as a promising approach to inhibit the process of metastatic UM cells. Pristimerin (PRI) has been demonstrated to inhibit the growth of several cancer cells, but its role and underlying mechanisms in the IGF-1-induced UM cell proliferation are largely unknown. The present study examined the anti-proliferative effect of PRI on UM cells and its possible role in IGF-1R signalling transduction. MTT and clonogenic assays were used to determine the role of PRI in the proliferation of UM cells. Flow cytometry was performed to detect the effect of PRI on the cell cycle distribution of UM cells. Western blotting was carried out to assess the effects of PRI and IGF-1 on the IGF-1R phosphorylation and its downstream targets. The results indicated that IGF-1 promoted the UM cell proliferation and improved the level of IGF-1R phosphorylation, whereas PRI attenuated the effect of IGF-1. Interestingly, PRI could not only induce the G1 phase accumulation and reduce the G2 phase induced by IGF-1, but also could stimulate the expression of p21 and inhibit the expression of cyclin D1. Besides, PRI could attenuate the phosphorylations of Akt, mTOR and ERK1/2 induced by IGF-1. Furthermore, the molecular docking study also demonstrated that PRI had potential inhibitory effects on IGF-1R. Taken together, these results indicated that PRI could inhibit the proliferation of UM cells through down-regulation of phosphorylated IGF-1R and its downstream signalling.
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