ArticleOncotarget2017
Reprogramming induced by isoliquiritigenin diminishes melanoma cachexia through mTORC2-AKT-GSK3β signaling.
Article in Oncotarget, 2017. 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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The trial behind it
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Who cites it
11 citing papers in PubMed, 24 citations in OpenAlex.
- Isoliquiritigenin: A natural compound with a promising role in inhibiting breast cancer lung metastasis.Journal of traditional and complementary medicine · 2025Article
- High expression of peroxisomal D-bifunctional protein in cytosol regulates apoptosis and energy metabolism of hepatocellular carcinoma cells via PI3K/AKT pathway.American journal of cancer research · 2023Article
- SGLT-2 Inhibitors in Cancer Treatment-Mechanisms of Action and Emerging New Perspectives.Cancers · 2022Review
- Tumor cell anabolism and host tissue catabolism-energetic inefficiency during cancer cachexia.Experimental biology and medicine (Maywood, N.J.) · 2022Article
- Role of mammalian target of rapamycin complex 2 in primary and secondary liver cancer.World journal of gastrointestinal oncology · 2021Review
- Perspectives on the Role of Isoliquiritigenin in Cancer.Cancers · 2021Review
- Alternative Options for Skin Cancer Therapy via Regulation of AKT and Related Signaling Pathways.International journal of molecular sciences · 2020Review
- Review
- Inhibition of mTORC2/RICTOR Impairs Melanoma Hepatic Metastasis.Neoplasia (New York, N.Y.) · 2018Article
- Isoliquiritigenin inhibits cell proliferation and migration through the PI3K/AKT signaling pathway in A549 lung cancer cells.Oncology letters · 2018Article
- Isoliquiritigenin suppresses human melanoma growth by targeting miR-301b/LRIG1 signaling.Journal of experimental & clinical cancer research : CR · 2018Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Isoliquiritigenin (ISL), a member of the flavonoids, is known to have anti-tumor activity in vitro and in vivo. The effect of ISL on reprogramming in cancer cells, however, remains elusive. In this study, we investigated the effect of ISL on reprogramming in human melanoma A375 cells. ISL (15 μg/ml) significantly inhibited A375 cell proliferation, anchorage independent cell proliferation and G2/M cell cycle arrest after ISL exposure for 24 h. However, there were no significant changes in apoptosis rate. Terminal differentiation indicators (melanin content, melanogenesis mRNA expression, tyrosinase (TYR) activity) were all up-regulated by ISL treatment. In ISL-treated cells, glucose uptake, lactate levels and mRNA expression levels of GLUT1 and HK2 were significantly decreased, and accompanied by an increase in O2 consumption rate (OCR) and adenosine triphosphate (ATP) deficiency. Protein expression levels of mTORC2-AKT-GSK3β signaling pathway components (mTOR, p-mTOR, RICTOR, p-AKT, p-GSK3β) decreased significantly after ISL treatment. Co-treatment of ISL and the mTOR-specific inhibitor Ku-0063794 had a synergistic effect on the inhibition of proliferation, and increased melanin content and TYR activity. Glucose uptake and lactate levels decreased more significantly than treatment with ISL alone. These findings indicate that ISL induced reprogramming in A375 melanoma cells by activating mTORC2-AKT-GSK3β signaling.
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