Department of Biological Sciences and Biotechnology, Faculty of Science and Technology, Universiti Kebangsaan Malaysia, 43600, Bangi, Selangor Darul Ehsan, Malaysia.
Department of Food Sciences, Faculty of Science and Technology, Universiti Kebangsaan Malaysia, 43600, Bangi, Selangor Darul Ehsan, Malaysia.
Sci Rep. 2021 Nov 30;11(1):23182. doi: 10.1038/s41598-021-02007-6.
Previous study has shown the antimicrobial activities of mucus protein extracted from Anabas testudineus. In this study, we are interested in characterizing the anticancer activity of the A. testudineus antimicrobial peptides (AMPs). The mucus was extracted, fractioned, and subjected to antibacterial activity testing to confirm the fish's AMPs production. The cytotoxic activity of each fraction was also identified. Fraction 2 (F2), which shows toxicity against MCF7 and MDA-MB-231 were sent for peptide sequencing to identify the bioactive peptide. The two peptides were then synthetically produced and subjected to cytotoxic assay to prove their efficacy against cancer cell lines. The IC for AtMP1 against MCF7 and MDA-MB-231 were 8.25 ± 0.14 μg/ml and 9.35 ± 0.25 μg/ml respectively, while for AtMP2 it is 5.89 ± 0.14 μg/ml and 6.97 ± 0.24 μg/ml respectively. AtMP1 and AtMP2 treatment for 48 h induced breast cancer cell cycle arrest and apoptosis by upregulating the p53, which lead to upregulate pro-apoptotic BAX gene and downregulate the anti-apoptotic BCL-2 gene, consequently, trigger the activation of the caspase-3. This interaction was supported by docking analysis (QuickDBD, HPEPDOCK, and ZDOCK) and immunoprecipitation. This study provided new prospects in the development of highly effective and selective cancer therapeutics based on antimicrobial peptides.
先前的研究表明,从 Anabas testudineus 中提取的黏液蛋白具有抗菌活性。在本研究中,我们有兴趣研究 A. testudineus 抗菌肽 (AMPs) 的抗癌活性。提取、分级并进行抗菌活性测试以确认鱼 AMPs 的产生。还确定了每个级分的细胞毒性活性。对 MCF7 和 MDA-MB-231 具有毒性的第 2 级分(F2)被送去进行肽测序以鉴定生物活性肽。然后合成这两种肽并进行细胞毒性测定,以证明它们对癌细胞系的功效。AtMP1 对 MCF7 和 MDA-MB-231 的 IC 分别为 8.25 ± 0.14 μg/ml 和 9.35 ± 0.25 μg/ml,而 AtMP2 的 IC 分别为 5.89 ± 0.14 μg/ml 和 6.97 ± 0.24 μg/ml。AtMP1 和 AtMP2 处理 48 小时通过上调 p53 诱导乳腺癌细胞周期停滞和凋亡,这导致上调促凋亡 BAX 基因和下调抗凋亡 BCL-2 基因,从而触发 caspase-3 的激活。这种相互作用得到了对接分析(QuickDBD、HPEPDOCK 和 ZDOCK)和免疫沉淀的支持。这项研究为基于抗菌肽开发高效和选择性癌症治疗提供了新的前景。