DT-13 inhibits the proliferation of pancreatic cancer by inducing apoptosis via AMPK-mTOR signaling

细胞凋亡 PI3K/AKT/mTOR通路 P70-S6激酶1 胰腺癌 安普克 细胞生长 癌症研究 信号转导 分子生物学 生物 污渍 流式细胞术 化学 细胞生物学 癌症 磷酸化 生物化学 基因 蛋白激酶A 遗传学
作者
Gangyin Xie,Fuyun Tong,Ming Xu,Siyu Yan,Ziwei Li
出处
期刊:Biochemical and Biophysical Research Communications [Elsevier]
卷期号:695: 149451-149451
标识
DOI:10.1016/j.bbrc.2023.149451
摘要

DT-13, the principal active component of Mysidium shortscapes from the Liliaceae family, has garnered substantial interest in cancer therapy owing to its potential anticancer properties. This study investigated the effects of DT-13 on the proliferation and apoptosis of human pancreatic cancer cell lines and aimed to elucidate the underlying mechanisms.PANC1 and CFPAC1 cells were exposed to DT-13 and their proliferation was assessed using RTCA and clone formation assays. Apoptotic protein expression was analyzed by western blotting, and apoptotic cells were identified by flow cytometry. RNA was extracted from DT-13 treated and untreated PANC1 cells for RNA sequencing. Differentially expressed genes were identified and subjected to GO bioprocess, KEGG pathway analysis, and western blotting. Finally, to evaluate tumor growth, CFPAC1 cells were subcutaneously injected into BALB/c nude mice.DT-13 inhibited proliferation and induced apoptosis of PANC1 and CFPAC1 cells by activating the AMPK/mTOR pathway and suppressing p70 S6K. Moreover, DT-13 hindered the growth of CFPAC1 xenograft tumors in nude mice.DT-13 effectively inhibited the growth of human pancreatic cancer cells.
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