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首页> 外文期刊>Cell biology international. >ERK1/2 and Akt pathway activated during (3R,6R)-bassiatin(1)-induced apoptosis in MCF-7 cells
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ERK1/2 and Akt pathway activated during (3R,6R)-bassiatin(1)-induced apoptosis in MCF-7 cells

机译：在（3R，6R）-bassiatin（1）诱导MCF-7细胞凋亡期间激活ERK1 / 2和Akt途径

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摘要

(3R,6R)-bassiatin(1) was isolated from the endogenous fungus, Fusarium oxysporum J8-1-2. Previous studies showed that (3R,6R)-bassiatin(1) has anti-oestrogen properties which make it cytotoxic to ER (oestrogen receptor)-positive breast cancer cells (MCF-7) by cell cycle arrest and induction of apoptosis. (3R,6R)-bassiatin(1) suppresses mRNA and protein expression of the ERα and oestrogen responsive genes of cyclin D1 and PR. We have investigated the interaction between (3R,6R)-bassiatin(1) and ERa and followed the roles of ERK (extracellular-signal-regulated kinase), Akt and GSK3β (glycogen synthase kinase 3β) during (3R,6R)-bassiatin(1)-induced apoptosis of MCF-7 cells. (3R,6R)-bassiatin(1) competed with E2 (17β-estradiol) for ERα active sites to inhibit ERα activation. However, while ERK1/2 and Akt were activated, GSK3β was inactivated during (3R,6R)-bassiatin(1)-induced apoptosis, suggesting that this compound is indeed an anti-oestrogen agent that can also activate the survival signalling pathway. Apoptosis caused by (3R,6R)-bassiatin(1) may be related to activation of ERK.
机译：（3R，6R）-bassatin（1）从内生真菌尖孢镰刀菌J8-1-2中分离出来。先前的研究表明（3R，6R）-bassatin（1）具有抗雌激素特性，可通过细胞周期停滞和诱导凋亡使其对ER（雌激素受体）阳性乳腺癌细胞（MCF-7）产生细胞毒性。 （3R，6R）-bassatin（1）抑制cyclin D1和PR的ERα和雌激素响应基因的mRNA和蛋白表达。我们研究了（3R，6R）-bassatin（1）与ERa之间的相互作用，并研究了（3R，6R）-bassatin中ERK（细胞外信号调节激酶），Akt和GSK3β（糖原合酶激酶3β）的作用（1）诱导MCF-7细胞凋亡。 （3R，6R）-basassiatin（1）与E2（17β-雌二醇）竞争ERα活性位点，从而抑制ERα激活。然而，虽然ERK1 / 2和Akt被激活，但在（3R，6R）-bassiatin（1）诱导的细胞凋亡期间，GSK3β被灭活，表明该化合物确实是一种抗雌激素剂，也可以激活生存信号通路。 （3R，6R）-bassatin（1）引起的细胞凋亡可能与ERK的激活有关。

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