Anisomycin sensitizes non‐small‐cell lung cancer cells to chemotherapeutic agents and epidermal growth factor receptor inhibitor via suppressing PI3K/Akt/mTOR

Tan, Hongxia; Hu, Biao; Xie, Fan; Zhu, Chuanbing; Cheng, Zhenshun

doi:10.1111/fcp.12641

Cited by 8 publications

(5 citation statements)

References 31 publications

(55 reference statements)

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“…Yang et al [59] reported that anisomycin inhibited the cell growth of breast cancer via AMPK activation and subsequent downstream inhibition of the mTOR. Tan et al [60] demonstrated that anisomycin had been shown to enhance the sensitivity of non-small-cell lung cancer cells to both chemotherapeutic agents and epidermal growth factor receptor (EGFR) inhibitors by suppressing the PI3K/Akt/mTOR signaling pathway.…”

Section: Resultsmentioning

confidence: 99%

A drug repurposing method based on inhibition effect on gene regulatory network

Li,

Liao,

Wang

et al. 2023

Computational and Structural Biotechnology Journal

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Section: Resultsmentioning

confidence: 99%

A drug repurposing method based on inhibition effect on gene regulatory network

Li,

Liao,

Wang

et al. 2023

Computational and Structural Biotechnology Journal

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“…Furthermore, how SLC7A11 regulates ferroptosis through a pathway other than GPX4 inactivation in HCC requires further investigation. In addition, the rescue of anisomycin-induced cell death by SB203580 was limited, because anisomycin (AN in figure) is a multifunctional drug that kills cells through multiple targets [77][78][79][80][81]. Moreover, several studies demonstrated that SB203580 could inhibit AKT, and the inhibition of AKT was involved in the induction of ferroptosis and apoptosis [82][83][84].…”

Section: Discussionmentioning

confidence: 99%

Modulation of the p38 MAPK Pathway by Anisomycin Promotes Ferroptosis of Hepatocellular Carcinoma through Phosphorylation of H3S10

Chen

Yang

Zhang

et al. 2022

Oxidative Medicine and Cellular Longevity

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Hepatocellular carcinoma (HCC) is a prevalent malignant tumor worldwide. Ferroptosis is emerging as an effective target for tumor treatment as it has been shown to potentiate cell death in some malignancies. However, it remains unclear whether histone phosphorylation events, an epigenetic mechanism that regulates transcriptional expression, are involved in ferroptosis. Our study found that supplementation with anisomycin, an agonist of p38 mitogen-activated protein kinase (MAPK), induced ferroptosis in HCC cells, and the phosphorylation of histone H3 on serine 10 (p-H3S10) was participated in anisomycin-induced ferroptosis. To investigate the anticancer effects of anisomycin-activated p38 MAPK in HCC, we analyzed cell viability, colony formation, cell death, and cell migration in Hep3B and HCCLM3 cells. The results showed that anisomycin could significantly suppress HCC cell colony formation and migration and induce HCC cell death. The hallmarks of ferroptosis, such as abnormal accumulation of iron and elevated levels of lipid peroxidation and malondialdehyde, were detected to confirm the ability of anisomycin to promote ferroptosis. Furthermore, coincubation with SB203580, an inhibitor of activated p38 MAPK, partially rescued anisomycin-induced ferroptosis. And the levels of p-p38 MAPK and p-H3S10 were successively increased by anisomycin treatment. The relationship between p-H3S10 and ferroptosis was revealed by ChIP sequencing. The reverse transcription PCR and immunofluorescence results showed that NCOA4 was upregulated both in mRNA and protein levels after anisomycin treatment. And by C11-BODIPY staining, we found that anisomycin-induced lipid reactive oxygen species was reduced after NCOA4 knockdown. In conclusion, the anisomycin-activated p38 MAPK promoted ferroptosis of HCC cells through H3S10 phosphorylation.

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“…Flavonoids had good antagonistic effect on three colorectal cancer cell lines (HCT116, HT‐29, and T84) [54]. Anisomycin inhibited the selective anti‐non‐small‐cell lung cancer activity via suppressing PI3K/Akt/mTOR [55].…”

Section: Biological Activitymentioning

confidence: 99%

Advances on pharmacology and toxicology of aconitine

Zhang

Liao

et al. 2022

Fundamemntal Clinical Pharma

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Aconitum alkaloids are considered to be the characteristic bioactive ingredients of Aconitum species, which are widely applied to the treatment of diverse diseases, and aconitine (AC) is found in most Aconitum plants.Research evidence shows that low-dose AC has a good therapeutic potential in heart failure, myocardial infarction, neuroinflammatory diseases, rheumatic diseases, and tumors, which has become one of the hotspots in global research in recent years. However, the cardiotoxicity and neurotoxicity of AC have also attracted extensive attention. Excessive use of AC always induces ventricular tachyarrhythmia and heart arrest, even can be potentially lethal. Therefore, AC cannot simply be regarded as a good medicine or a toxicant, but its underlying curative and toxic properties remained chaos. In order to dig the unique pharmacological value of AC while preventing its toxicity, the pharmacological activities and toxic effects of AC were summarized in this paper, providing new insight into the safe and effective use of AC in clinical practice.

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Anisomycin sensitizes non‐small‐cell lung cancer cells to chemotherapeutic agents and epidermal growth factor receptor inhibitor via suppressing PI3K/Akt/mTOR

Cited by 8 publications

References 31 publications

A drug repurposing method based on inhibition effect on gene regulatory network

A drug repurposing method based on inhibition effect on gene regulatory network

Modulation of the p38 MAPK Pathway by Anisomycin Promotes Ferroptosis of Hepatocellular Carcinoma through Phosphorylation of H3S10

Advances on pharmacology and toxicology of aconitine

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