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open-access-imgOpen AccessMarine toxin (+)‐chaetocin‐induced apoptosis of lung large cell carcinoma cell lines through cell cycle arrest via CDKN1A expression and replicative stress
Author(s)
Qian Mengjia,
Cao Xin
Publication year2022
Publication title
clinical and translational discovery
Resource typeJournals
PublisherWiley
Abstract Lung large cell carcinoma is a common type of lung cancer with poor prognosis. Although targeted drugs have achieved enormous success in treating non‐small‐cell lung carcinoma (NSCLC), new chemotherapy is needed since the emerged drug resistance always hinders curative effects. The fungal toxin (+)‐chaetocin demonstrated strong antineoplastic activities against the tested lung large cell carcinoma cell lines H460 and H661 at submicromolar concentrations. Further research demonstrated that (+)‐chaetocin effectively induced H460 apoptosis at 10–30 nM concentrations, while cell death occurred at 60 nM concentrations due to DNA duplication errors. Cell cycle and transcriptional analyses proved that cell cycle arrest via CDKN1A expression and the comprehensive replicative stress of (+)‐chaetocin are key factors in the (+)‐chaetocin working mechanisms.
Subject(s)apoptosis , biochemistry , biology , cancer research , cell , cell culture , cell cycle , cell cycle checkpoint , cell growth , chemistry , dna , dna damage , genetics , lung cancer , medicine , microbiology and biotechnology , programmed cell death
Language(s)English
ISSN2768-0622
DOI10.1002/ctd2.49

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