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甲基山柰酰胺通过调节增殖、凋亡和转移能力，在结肠癌细胞中发挥抗肿瘤作用。

-methylsansalvamide elicits antitumor effects in colon cancer cells and by regulating proliferation, apoptosis, and metastatic capacity.

作者信息

Park Juhee, Moon Sung-Kwon, Lee Chan

机构信息

Food Analysis Research Center, Food Industry Research Division, Korea Food Research Institute, Wanju, Republic of Korea.

Department of Food Science and Biotechnology, Chung-Ang University, Anseong, Republic of Korea.

出版信息

Front Pharmacol. 2023 Mar 16;14:1146966. doi: 10.3389/fphar.2023.1146966. eCollection 2023.

DOI:10.3389/fphar.2023.1146966
PMID:37007044
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10060634/
Abstract

-methylsansalvamide (MSSV), a cyclic pentadepsipeptide, was obtained from a strain of f. radicicola. The current study investigated the anti-colorectal cancer effect of MSSV. MSSV exhibited the inhibition of the proliferation in HCT116 cells induction of G0/G1 cell cycle arrest by downregulating CDK 2, CDK6, cyclin D, and cyclin E, and upregulating p21WAF1 and p27KIP1. Decreased phosphorylation of AKT was observed in MSSV-treated cells. Moreover, MSSV treatment induced caspase-mediated apoptosis through elevating the level of cleaved caspase 3, cleaved PARP, cleaved caspase 9, and pro-apoptotic Bax. MSSV revealed the declined MMP-9 level mediated by reduction in the binding activity of AP-1, Sp-1, and NF-κB motifs, which led to the migration and invasion of HCT116 cells. metabolism with rat liver S9 fractions was performed to examine the effect of MSSV metabolites. The metabolic process enhanced the inhibitory effect of MSSV on the HCT116 cell proliferation decline of cyclin D1 expression and AKT phosphorylation. Finally, oral administration of MSSV inhibited the tumor growth of HCT116 xenograft mice. These results suggest that MSSV is a potential anti-tumor agent in colorectal cancer treatment.

摘要

甲基桑萨酰胺（MSSV）是一种环状五肽缩酚酸肽，从一种放射状根瘤菌菌株中获得。本研究调查了MSSV的抗结直肠癌作用。MSSV表现出对HCT116细胞增殖的抑制作用，通过下调细胞周期蛋白依赖性激酶2（CDK 2）、细胞周期蛋白依赖性激酶6（CDK6）、细胞周期蛋白D和细胞周期蛋白E，并上调p21WAF1和p27KIP1来诱导G0/G1期细胞周期阻滞。在MSSV处理的细胞中观察到AKT磷酸化水平降低。此外，MSSV处理通过提高裂解的半胱天冬酶3、裂解的聚（ADP-核糖）聚合酶（PARP）、裂解的半胱天冬酶9和促凋亡蛋白Bax的水平诱导半胱天冬酶介导的凋亡。MSSV显示，由于AP-1、Sp-1和NF-κB基序的结合活性降低，导致MMP-9水平下降，进而导致HCT116细胞的迁移和侵袭。用大鼠肝脏S9组分进行代谢研究，以检查MSSV代谢产物 的作用。代谢过程增强了MSSV对HCT116细胞增殖的抑制作用，以及细胞周期蛋白D1表达和AKT磷酸化的下降。最后，口服MSSV可抑制HCT116异种移植小鼠的肿瘤生长。这些结果表明，MSSV是结直肠癌治疗中一种潜在的抗肿瘤药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/098a/10060634/003b7bd65e13/fphar-14-1146966-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/098a/10060634/8cd53f29a5a2/fphar-14-1146966-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/098a/10060634/17e8ebf1e736/fphar-14-1146966-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/098a/10060634/4b3d8825a6d6/fphar-14-1146966-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/098a/10060634/dd20f508a349/fphar-14-1146966-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/098a/10060634/1f53330b5dd6/fphar-14-1146966-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/098a/10060634/8523b46ac53b/fphar-14-1146966-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/098a/10060634/025cbbdb579c/fphar-14-1146966-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/098a/10060634/003b7bd65e13/fphar-14-1146966-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/098a/10060634/8cd53f29a5a2/fphar-14-1146966-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/098a/10060634/17e8ebf1e736/fphar-14-1146966-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/098a/10060634/4b3d8825a6d6/fphar-14-1146966-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/098a/10060634/dd20f508a349/fphar-14-1146966-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/098a/10060634/1f53330b5dd6/fphar-14-1146966-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/098a/10060634/8523b46ac53b/fphar-14-1146966-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/098a/10060634/025cbbdb579c/fphar-14-1146966-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/098a/10060634/003b7bd65e13/fphar-14-1146966-g008.jpg

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