Cochlioquinone derivatives with apoptosis-inducing effects on HCT116 colon cancer cells from the phytopathogenic fungus Bipolaris luttrellii L439. | LitMetric
State Key Laboratory of Mycology, Institute of Microbiology, Chinese Academy of Sciences, No. 1 Beichen West Road, Chaoyang District, Beijing 100101, P. R. China, (phone/fax: +86-10-64806074); University of Chinese Academy of Sciences, Yu Quan Lu 19, Shijingshan District, Beijing 100049, P. R. China.
Published: December 2014
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Article Abstract
A new cochlioquinone derivative, cochlioquinone F (1), as well as three known compounds, anhydrocochlioquinone A (2), isocochlioquinone A (3), and isocochlioquinone C (4), were isolated from the PDB (potato dextrose broth) culture of the phytopathogenic fungus Bipolaris luttrellii. The structure of 1 was elucidated on the basis of NMR techniques. The apoptosis-inducing effects of compounds 1-4 were evaluated against HCT116 cancer cells. Compound 2 exhibited the strongest activity in inducing apoptosis on HCT116 cells within the range of 10-30 μM. In addition, the caspase activation, the release of cytochrome c from mitochondria, and the downregulation of Bcl-2 protein in HCT116 cells treated with compound 2 were detected.
The TGFβ signaling pathway is known for its pleiotropic functions in a plethora of biological processes. In melanoma, TGFβ signaling promotes invasiveness and metastasis formation. However, its involvement in the response to therapy is controversial.
School of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou, China; Zhejiang Key Laboratory of Chinese Medicine for Cardiovascular and Cerebrovascular Disease, Hangzhou, China. Electronic address:
Ethnopharmacological Relevance: The combination of Astragalus membranaceus (Huang Qi in Chinese, HQ) and Carthamus tinctorius (Hong Hua in Chinese, HH) is commonly employed for treating ischemic stroke (IS). The heavily oxidative environment of cerebral ischemia/reperfusion injury (CI/RI) promotes activation of poly (ADP-ribose) polymerase-1 (PARP-1), which initiates parthanatos, a regulated cell death mode. Reactive oxygen species (ROS) bursting in mitochondrial respiratory chain complex I (Complex I) is a key cause of CI/RI.
Drugs that eliminate senescent cells, senolytics, can be powerful when combined with prosenescence cancer therapies. Using a CRISPR/Cas9-based genetic screen, we identify here SLC25A23 as a vulnerability of senescent cancer cells. Suppressing SLC25A23 disrupts cellular calcium homeostasis, impairs oxidative phosphorylation, and interferes with redox signaling, leading to death of senescent cells.
Background: Disulfidptosis has recently emerged as a novel form of regulated cell death (RCD). Evasion of cell death is a hallmark of cancer, and the resistance of many tumors to apoptosis-inducing therapies has heightened interest in exploring alternative RCD mechanisms.
Methods: Transcriptomic and clinical data were obtained from The Cancer Genome Atlas (TCGA), Genotype-Tissue Expression (GTEx), and Chinese Glioma Genome Atlas (CGGA).
Inducing programmed cell death in tumors is a fundamental approach in cancer therapy, prompting extensive efforts to discover bioactive compounds with anticancer properties. , a plant used in traditional medicine across East Asia, has been reported to exhibit various biological activities, including anticancer effects. This study aimed to evaluate the apoptosis-inducing effects of methanol/dichloromethane (MeOH/CHCl) extracts of roots and their components in HL-60 human leukemia cells.
