ArticleFrontiers in pharmacology2022
β-elemene Isopropanolamine Derivative LXX-8250 Induces Apoptosis Through Impairing Autophagic Flux
Article in Frontiers in pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
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Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Research progress of Chinese medicinal monomers in the process of melanoma occurrence.Pharmaceutical biology · 2025Pooled it
- Effects of Citrus-derived Diosmetin on Melanoma: Induction of Apoptosis and Autophagy Mediated by PI3K/Akt/mTOR Pathway Inhibition.Anti-cancer agents in medicinal chemistry · 2025Article
- Elemene Antitumor Drugs Development Based on "Molecular Compatibility Theory" and Clinical Application: A Retrospective and Prospective Outlook.Chinese journal of integrative medicine · 2024Review
- Targeting programmed cell death via active ingredients from natural plants: a promising approach to cancer therapy.Frontiers in pharmacology · 2024Review
- HILPDA Repression Induces Methuosis in Breast and Liver Cancer Cells by Dysregulating Lipid Metabolism.BioFactors (Oxford, England)Article
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Authors and funding
10 authors.
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Abstract
Melanoma is a highly aggressive skin cancer and accounts for most of the skin cancer-related deaths. The efficacy of current therapies for melanoma remains to be improved. The isopropanolamine derivative of β-elemene LXX-8250 was reported to present better water solubility and stronger toxicity to tumor cells than β-elemene. Herein, LXX-8250 treatment showed 4-5-fold more toxicity to melanoma cells than the well-known anti-melanoma drug, Dacarbazine. LXX-8250 treatment induced apoptosis remarkably, which was caused by the impairment of autophagic flux. To clarify the molecular mechanism, microarray analyses were conducted, and PFKFB4 expression was found to be suppressed by LXX-8250 treatment. The cells overexpressed with PFKFB4 exhibited resistance to apoptosis induction and autophagic flux inhibition by LXX-8250 treatment. Moreover, LXX-8250 treatment suppressed glycolysis, to which the cells overexpressed with PFKFB4 were tolerant. LXX-8250 treatment inhibited the growth of melanoma xenografts and suppressed PFKFB4 expression and glycolysis
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