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人参皂苷 Rg1 通过抑制 Akt/mTOR/p70S6K 通路诱导结直肠癌细胞自噬。

Ginsenoside Rg1 Induces Autophagy in Colorectal Cancer through Inhibition of the Akt/mTOR/p70S6K Pathway.

机构信息

Jiangsu Province Academy of Traditional Chinese Medicine, 210028 Nanjing, Jiangsu Province, P.R. China.

Nanjing Lishui District Hospital of Traditional Chinese Medicine, 211200 Nanjing, Jiangsu Province, P.R. China.

出版信息

J Microbiol Biotechnol. 2024 Apr 28;34(4):774-782. doi: 10.4014/jmb.2310.10043. Epub 2024 Jan 12.

DOI:10.4014/jmb.2310.10043
PMID:38668684
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11091659/
Abstract

This study aimed to elucidate the anti-colon cancer mechanism of ginsenoside Rg1 in vitro and in vivo. Cell viability rate was detected using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) tetrazolium assay. The inhibitory effect of ginsenoside Rg1 against CT26 cell proliferation gradually increased with increasing concentration. The in vivo experiments also demonstrated an antitumor effect. The monodansylcadaverine (MDC), transmission electron microscopy (TEM), and expression of autophagy marker proteins confirmed that ginsenoside Rg1 induced autophagy in vitro. Ginsenoside Rg1 induced autophagy death of CT26 cells, but this effect could be diminished by autophagy inhibitor (3-methyladenine, 3-MA). Additionally, in a xenograft model, immunohistochemical analysis of tumor tissues showed that the LC3 and Beclin-1 proteins were highly expressed in the tumors from the ginsenoside Rg1-treated nude mice, confirming that ginsenoside Rg1 also induced autophagy in vivo. Furthermoer, both in vivo and in vitro, the protein expressions of p-Akt, p-mTOR, and p-p70S6K were inhibited by ginsenoside Rg1, which was verified by Akt inhibitors. These results indicated that the mechanism of ginsenoside Rg1 against colon cancer was associated with autophagy through inhibition of the Akt/mTOR/p70S6K signaling pathway.

摘要

本研究旨在体外和体内阐明人参皂苷 Rg1 的抗结肠癌机制。采用 3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四氮唑溴盐（MTT）比色法检测细胞活力。人参皂苷 Rg1 对 CT26 细胞增殖的抑制作用随浓度的增加逐渐增强。体内实验也证实了其抗肿瘤作用。单丹磺酰尸胺（MDC）、透射电子显微镜（TEM）和自噬标志物蛋白的表达证实，人参皂苷 Rg1 在体外诱导自噬。人参皂苷 Rg1 诱导 CT26 细胞自噬死亡，但这种作用可被自噬抑制剂（3-甲基腺嘌呤，3-MA）减弱。此外，在异种移植模型中，肿瘤组织的免疫组化分析显示，人参皂苷 Rg1 处理的裸鼠肿瘤中 LC3 和 Beclin-1 蛋白表达水平较高，证实人参皂苷 Rg1 也在体内诱导自噬。此外，无论是在体内还是体外，人参皂苷 Rg1 均可抑制 Akt/mTOR/p70S6K 信号通路，从而抑制 p-Akt、p-mTOR 和 p-p70S6K 的蛋白表达，这一结果得到 Akt 抑制剂的验证。这些结果表明，人参皂苷 Rg1 抗结肠癌的机制与通过抑制 Akt/mTOR/p70S6K 信号通路诱导自噬有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f309/11091659/605e78bf667d/jmb-34-4-774-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f309/11091659/a8832421eebc/jmb-34-4-774-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f309/11091659/4b2a957dfeaf/jmb-34-4-774-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f309/11091659/963eb1109c6a/jmb-34-4-774-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f309/11091659/c3691d9e03ad/jmb-34-4-774-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f309/11091659/fba28d31b4c3/jmb-34-4-774-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f309/11091659/605e78bf667d/jmb-34-4-774-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f309/11091659/a8832421eebc/jmb-34-4-774-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f309/11091659/4b2a957dfeaf/jmb-34-4-774-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f309/11091659/963eb1109c6a/jmb-34-4-774-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f309/11091659/c3691d9e03ad/jmb-34-4-774-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f309/11091659/fba28d31b4c3/jmb-34-4-774-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f309/11091659/605e78bf667d/jmb-34-4-774-f6.jpg

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