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华通氏胶间充质干细胞来源条件培养基通过激活 AMPK/mTOR 介导的自噬对结肠癌细胞的抑制作用

英文原题:Wharton's jelly mesenchymal stem cell-derived conditioned media inhibits colon cancer cells via activating AMPK/mTOR-mediated autophagy.

查看英文原题

Wharton's jelly mesenchymal stem cell-derived conditioned media inhibits colon cancer cells via activating AMPK/mTOR-mediated autophagy.

PubMed 2026/01/01(内容时间) Mol Biol Res Commun Q4 · IF 1.4(JCR 2025)

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中文摘要

先前的研究表明,来源于沃顿胶间充质干细胞的条件培养基(WJ-CM)具有抗癌特性。本研究通过检测自噬生物标志物和AMPK/mTOR通路,探讨了WJ-CM对HT-29结直肠腺癌细胞的影响。将HT-29细胞暴露于WJ-CM和AMPK激活剂(AICAR)。研究了自噬以及AMPK和mTOR蛋白的水平。WJ-CM增加了HT-29细胞中磷酸化AMPK的表达,同时降低了磷酸化mTOR的水平。WJ-CM处理提高了LC3B/LC3A比值以及ATG7、ATG5和Beclin-1的表达。然而,p62表达同时下降,这表明自噬被诱导。AICAR增强了WJ-CM对HT-29细胞活力的影响,以及自噬相关生物标志物、磷酸化AMPK和磷酸化mTOR的水平。WJ-CM通过激活AMPK/mTOR介导的自噬抑制结直肠癌细胞生长。

展开英文摘要原文

Prior studies have shown that conditioned media derived from Wharton's jelly mesenchymal stem cells (WJ-CM) have anti-cancer properties. This research investigated the impact of WJ-CM on HT-29 colorectal adenocarcinoma cells by examining autophagy biomarkers and the AMPK/mTOR pathway.

The HT-29 cells were subjected to WJ-CM and an AMPK activator (AICAR). Autophagy and levels of AMPK and mTOR proteins were investigated. WJ-CM increased the expression of phosphorylated AMPK while reducing the level of phosphorylated mTOR in HT-29 cells. WJ-CM treatment elevated the LC3B/LC3A ratio and ATG7, ATG5, and Beclin-1 expression.

However, there was a parallel drop in p62 expression, which indicates autophagy induction. AICAR increased the influence of WJ-CM on viability, as well as the levels of biomarkers associated with autophagy, phosphorylated AMPK, and phosphorylated mTOR in the HT-29 cells. WJ-CM inhibits colorectal cancer cell growth via activating AMPK/mTOR-mediated autophagy.

论文信息

作者
Dayer D、Akbari-Jonoush Z、Mahdavi R、Amari A、Keshavarz-Zarjani A、Khorsandi L
单位
Cellular and Molecular Research Center, Medical Basic Sciences Research Institute, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.Iran
期刊
Molecular biology research communications2026
原文标识
PubMed 41346764 · DOI 10.22099/mbrc.2025.52891.2133