ArticlePreventive nutrition and food science2023
Harmine Hydrochloride Induces G2/M Cell Cycle Arrest and Apoptosis in SK-Hep1 Hepatocellular Carcinoma Cells by Regulating Mitogen-Activated Protein Kinases and the PI3K/AKT Pathway.
Article in Preventive nutrition and food science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 4 citations in OpenAlex.
- Harmine Hydrochloride fromPharmaceuticals (Basel, Switzerland) · 2026Article
- Harmine suppresses the malignant phenotypes of Lewis lung carcinoma cells by inhibiting EGFR phosphorylation.American journal of translational research · 2026Article
- Targeting Chemical-induced Hepatocellular Carcinoma: Ameliorative Potential of Natural Compounds with Focus on Beta-carbolines.Mini reviews in medicinal chemistry · 2026Review
- Mitochondrial dysfunction in hepatocellular carcinoma: from metabolism to targeted therapies.Molecular and cellular biochemistry · 2025Review
- Harmine derivative H-2-168 induces the death ofPharmaceutical biology · 2025Article
- Harmine hydrochloride induces G0/G1 cell cycle arrest and apoptosis in oral squamous carcinoma cells.Experimental and therapeutic medicine · 2025Article
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Authors and funding
1 author at 1 institution in 1 country.
Funding
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Abstract
Liver cancer is a globally common form of cancer. Thus, novel drugs derived from natural products are needed to reduce the side effects of chemotherapy. The present study aimed to analyze the anticancer properties and effects of harmine hydrochloride (HMH), a water-soluble metabolite of harmine that can be easily absorbed into tissues, in treating liver cancer cells. HMH dose-dependently inhibited cell growth, migration, invasion, and colony formation in SK-Hep1 cells. It also induced G2/M arrest by reducing the expression of p-cdc2, cyclin B1, and Rb (G2/M phase regulatory proteins) in a dose-dependent manner. HMH treatment reduced the expression of caspase-9, caspase-3, PARP, and Bcl-2 and increased the expression of Bax (a proapoptotic protein). Moreover, it increased the production of reactive oxygen species and decreased the intracellular uptake of rhodamine 123 due to mitochondrial dysfunction because of oxidative stress. HMH treatment also upregulated the phosphorylation of JNK, p38, and FOXO3a in SK-Hep1 cells and downregulated the PI3K/AKT signaling pathway. Our findings suggest that HMH may activate the compounds responsible for anticancer effects in hepatocellular carcinoma cells.
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