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探讨鱼骨发酵物的抗癌作用:诱导人结肠癌细胞凋亡和自噬。

Exploring the Anti-Cancer Effects of Fish Bone Fermented Using : Induction of Apoptosis and Autophagy in Human Colorectal Cancer Cells.

机构信息

Department of Seafood Science, National Kaohsiung University of Science and Technology, Kaohsiung 81157, Taiwan.

Department of Chemical and Materials Engineering, National Kaohsiung University of Science and Technology, Kaohsiung 80778, Taiwan.

出版信息

Molecules. 2023 Jul 27;28(15):5679. doi: 10.3390/molecules28155679.

DOI:10.3390/molecules28155679
PMID:37570647
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10419882/
Abstract

Fish bone fermented using (FBF) has total phenols and functional amino acids that contribute to its anti-oxidant and anti-inflammatory properties. Colorectal cancer, one of the most prevalent cancers and the third largest cause of death worldwide, has become a serious threat to global health. This study investigates the anti-cancer effects of FBF (1, 2.5 or 5 mg/mL) on the cell growth and molecular mechanism of HCT-116 cells. The HCT-116 cell treatment with 2.5 or 5 mg/mL of FBF for 24 h significantly decreased cell viability ( < 0.05). The S and G2/M phases significantly increased by 88-105% and 25-43%, respectively ( < 0.05). Additionally, FBF increased the mRNA expression of caspase 8 (38-77%), protein expression of caspase 3 (34-94%), poly (ADP-ribose) polymerase (PARP) (31-34%) and induced apoptosis (236-773%) of HCT-116 cells ( < 0.05). FBF also increased microtubule-associated protein 1B light chain 3 (LC3) (38-48%) and phosphoinositide 3 kinase class III (PI3K III) (32-53%) protein expression, thereby inducing autophagy (26-52%) of HCT-116 cells ( < 0.05). These results showed that FBF could inhibit HCT-116 cell growth by inducing S and G2/M phase arrest of the cell cycle, apoptosis and autophagy. Thus, FBF has the potential to treat colorectal cancer.

摘要

鱼骨经发酵后(FBF)含有总酚类化合物和功能性氨基酸,具有抗氧化和抗炎特性。结直肠癌是全球最常见的癌症之一,也是全球第三大死亡原因,已成为全球健康的严重威胁。本研究探讨了 FBF(1、2.5 或 5mg/mL)对 HCT-116 细胞生长的抗癌作用及其分子机制。用 2.5 或 5mg/mL 的 FBF 处理 HCT-116 细胞 24 小时后,细胞活力显著降低(<0.05)。S 和 G2/M 期分别显著增加了 88-105%和 25-43%(<0.05)。此外,FBF 增加了 caspase 8 的 mRNA 表达(38-77%)、caspase 3 的蛋白表达(34-94%)、多聚(ADP-核糖)聚合酶(PARP)(31-34%),并诱导了 HCT-116 细胞的凋亡(236-773%)(<0.05)。FBF 还增加了微管相关蛋白 1B 轻链 3(LC3)(38-48%)和磷酸肌醇 3 激酶 III(PI3K III)(32-53%)蛋白的表达,从而诱导了 HCT-116 细胞的自噬(26-52%)(<0.05)。这些结果表明,FBF 可通过诱导细胞周期的 S 和 G2/M 期阻滞、细胞凋亡和自噬来抑制 HCT-116 细胞的生长。因此,FBF 具有治疗结直肠癌的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd5e/10419882/78aa592c0d1c/molecules-28-05679-g006.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd5e/10419882/6ab7e2f671da/molecules-28-05679-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd5e/10419882/265aa4a81662/molecules-28-05679-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd5e/10419882/1d465d764485/molecules-28-05679-g003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd5e/10419882/78aa592c0d1c/molecules-28-05679-g006.jpg

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