ArticleEvidence-based complementary and alternative medicine : eCAM2013
Induction of apoptosis by luteolin involving akt inactivation in human 786-o renal cell carcinoma cells.
Article in Evidence-based complementary and alternative medicine : eCAM, 2013. 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, 27 citations in OpenAlex.
- Advances in the Mechanism of Luteolin against Hepatocellular Carcinoma Based on Bioinformatics and Network Pharmacology.Journal of Cancer · 2023Review
- Review
- HO-1 Contributes to Luteolin-Triggered Ferroptosis in Clear Cell Renal Cell Carcinoma via Increasing the Labile Iron Pool and Promoting Lipid Peroxidation.Oxidative medicine and cellular longevity · 2022Article
- Role of protein phosphatase 2A in kidney disease (Review).Experimental and therapeutic medicine · 2021Review
- Traditional Chinese medicines and their active ingredients sensitize cancer cells to TRAIL-induced apoptosis.Journal of Zhejiang University. Science. B · 2021Review
- Protective effects of apigenin on altered lipid peroxidation, inflammation, and antioxidant factors in methotrexate-induced hepatotoxicity.Naunyn-Schmiedeberg's archives of pharmacology · 2021Article
- Endoplasmic Reticulum Stress Contributes to Indomethacin-Induced Glioma Apoptosis.International journal of molecular sciences · 2020Article
- Molecular targets of luteolin in cancer.European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP) · 2016Review
- Cytotoxicity of dietary flavonoids on different human cancer types.Pharmacognosy reviews · 2014Review
Corrections and comments
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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
There is a growing interest in the health-promoting effects of natural substances obtained from plants. Although luteolin has been identified as a potential therapeutic and preventive agent for cancer because of its potent cancer cell-killing activity, the molecular mechanisms have not been well elucidated. This study provides evidence of an alternative target for luteolin and sheds light on the mechanism of its physiological benefits. Treatment of 786-O renal cell carcinoma (RCC) cells (as well as A498 and ACHN) with luteolin caused cell apoptosis and death. This cytotoxicity was caused by the downregulation of Akt and resultant upregulation of apoptosis signal-regulating kinase-1 (Ask1), p38, and c-Jun N-terminal kinase (JNK) activities, probably via protein phosphatase 2A (PP2A) activation. In addition to being a concurrent substrate of caspases and event of cell death, heat shock protein-90 (HSP90) cleavage might also play a role in driving further cellular alterations and cell death, at least in part, involving an Akt-related mechanism. Due to the high expression of HSP90 and Akt-related molecules in RCC and other cancer cells, our findings suggest that PP2A activation might work in concert with HSP90 cleavage to inactivate Akt and lead to a vicious caspase-dependent apoptotic cycle in luteolin-treated 786-O cells.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.