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- Ethyl β-carboline-3-carboxylate increases cervical cancer cell apoptosis through ROS-p38 MAPK signaling pathway
- H N Sun; D P Xie; C X Ren; X Y Guo; H N Zhang; W Q Xiao; Y H Han; Y D Cui; Taeho Kwon
- Bibliographic Citation
- in Vivo, vol. 36, no. 3, pp. 1178-1187
- Publication Year
- Background/aim: Ethyl β-carboline-3-carboxylate (β-CCE) is one of the effective ingredients of Picrasma quassioides (P. quassioides). As a β-carboline alkaloid, it can antagonize the pharmacological effects of benzodiazepines by regulating neurotransmitter secretion through receptors, thus affecting anxiety and physiology. However, its efficacy in cancer treatment is still unclear.
Materials and methods: We explored the effect of b-CCE on SiHa cells using MTT assay, western blot, flow cytometry, LDH release, T-AOC, SOD, and MDA assays.
Results: We investigated the cytotoxicity of β-CCE in SiHa cells and verified that β-CCE could induce cell apoptosis in a time- and concentration-dependent manner. In this process, treatment with β-CCE significantly increased the levels of cytoplasmic and mitochondrial reactive oxygen species (ROS), which disturb the oxidation homeostasis by regulating the total antioxidant capacity (T-AOC), superoxide dismutase (SOD) activity, and malondialdehyde (MDA) production. Notably, the addition of N-acetylcysteine (NAC) (ROS scavenger) effectively alleviated β-CCE-induced apoptosis in SiHa cells. In addition, β-CCE might activate the p38/MAPK signaling pathway, as the pre-treatment with SB203580 (p38 inhibitor) significantly reduced β-CCE-induced apoptosis in SiHa cells.
Conclusion: β-CCE has an anti-tumor activity. It activates the p38/MAPK signaling pathway by increasing intracellular ROS levels, which subsequently induce SiHa cell apoptosis. Our results provide a novel therapeutic target for treatment of cervical cancer.
- Apoptosisp38 signaling pathwayCervical cancerEthyl β-carboline-3-carboxylateOxidative stress
- Int Inst Anticancer Research
- Appears in Collections:
- Jeonbuk Branch Institute > Primate Resources Center > 1. Journal Articles
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