RNF43 p.G659fs 通过 PI3K/AKT/mTOR 信号通路和 HLA-E 上调导致 MSI-high 结直肠癌中 NK 细胞功能障碍
RNF43 p.G659fs leads to natural killer cell dysfunction in MSI-high colorectal cancer through PI3K/AKT/mTOR signaling and HLA-E up-regulation.
CELL INTELLIGENCE · 肿瘤细胞治疗研究
肿瘤细胞治疗研究
英文原题:Wharton's jelly mesenchymal stem cell-derived conditioned media inhibits colon cancer cells via activating AMPK/mTOR-mediated autophagy.
Wharton's jelly mesenchymal stem cell-derived conditioned media inhibits colon cancer cells via activating AMPK/mTOR-mediated autophagy.
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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。
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.
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