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首页> 外文期刊>Cell biology international. >Rhabdastrellic acid-A inhibited PI3K/Akt pathway and induced apoptosis in human leukemia HL-60 cells
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Rhabdastrellic acid-A inhibited PI3K/Akt pathway and induced apoptosis in human leukemia HL-60 cells

机译：鼠李糖醛酸-A抑制人白血病HL-60细胞的PI3K / Akt通路并诱导其凋亡

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摘要

Increasing evidence suggests that aberrant activation of PI3K/Akt is involved in many human cancers, and that inhibition of the PI3K/Akt pathway might be a promising strategy for cancer treatment. Our investigation indicates that Rhabdastrellic acid-A, an isomalabaricane triterpenoid isolated from the sponge, Rhabdastrella globostellata, inhibits proliferation of HL-60 cells with an IC50 value of 0.68 μg/ml, and induces apoptosis. Rhabdastrellic acid-A also induces cleavage of the death substrate poly (ADP-ribose) polymerase (PARP) and caspase-3. Pretreatment of HL-60 cells with the caspase-3 specific inhibitor, DEVD-CHO, prevents Rhabdastrellic acid-A-induced DNA fragmentation and PARP cleavage. Activated PI3K and Akt significantly decreases after treatment with Rhabdastrellic acid-A in HL-60 cells. Expression levels of protein bcl-2, bax remain unchanged in response to Rhabdastrellic acid-A treatment in HL-60 cells. These results suggest that Rhabdastrellic acid-A inhibits PI3K/Akt pathway and induces caspase-3 dependent-apoptosis in HL-60 human leukemia cells.
机译：越来越多的证据表明，PI3K / Akt的异常激活与许多人类癌症有关，并且抑制PI3K / Akt途径可能是一种有前途的癌症治疗策略。我们的研究表明，Rhabdastrellic acid-A，一种从海绵中分离出的异巴拉巴烷三萜，Rhabdastrella globostellata，抑制HL-60细胞的增殖，IC50值为0.68μg/ ml，并诱导凋亡。 Rhabdastrellic acid-A还诱导死亡底物聚（ADP-核糖）聚合酶（PARP）和caspase-3的裂解。用caspase-3特异性抑制剂DEVD-CHO预处理HL-60细胞可防止Rhabdastrellic acid-A诱导的DNA片段化和PARP裂解。 Rhabdastrellic acid-A处理HL-60细胞后，活化的PI3K和Akt明显降低。在HL-60细胞中，对Rhabdastrellic acid-A处理后，蛋白bcl-2，bax的表达水平保持不变。这些结果表明，Rhabdastrellic acid-A抑制HL-60人白血病细胞中的PI3K / Akt途径并诱导caspase-3依赖性凋亡。

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