海棠乙酸乙酯提取物诱导结直肠癌细胞凋亡、自噬和细胞周期阻滞。

IF 1.6 Q3 FOOD SCIENCE & TECHNOLOGY
Pathanin Chantree, Pongsakorn Martviset, Phornphan Sornchuer, Nattaya Thongsepee, Kant Sangpairoj, Krai Meemon, Nakorn Niamnont, Montakan Tamtin, Prasert Sobhon
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引用次数: 0

摘要

结直肠癌是最致命的癌症之一。然而,传统的癌症治疗仍然有副作用。因此,目前仍在寻找副作用较小的新型化疗药物。一种海洋红海藻,Halymenia durvillei,最近对其抗癌作用很感兴趣。本研究通过磷酸肌肽3-激酶(PI3K)/蛋白激酶B (AKT)/哺乳动物雷帕霉素靶蛋白(mTOR)信号通路,探讨了苦参乙酸乙酯提取物(HDEA)对HT-29结直肠癌细胞的抗癌作用。采用3-(4,5-二甲基-2-噻唑基)-2,5-二苯基溴化四氮唑法检测经hdea处理的HT-29和OUMS-36细胞的细胞活力。观察HDEA对细胞凋亡和细胞周期的影响。采用Hoechst 33342染色和JC-1染色分别观察细胞核形态和线粒体膜电位(ΔΨm)。采用实时半定量逆转录聚合酶链反应检测PI3K、AKT和mTOR基因的表达。western blot检测相应蛋白的表达。结果显示,处理后的HT-29细胞的细胞活力下降,而OUMS-36细胞的细胞活力无明显下降。通过下调细胞周期蛋白依赖性ki-nase 4和细胞周期蛋白D1, hdea处理的HT-29细胞被阻滞在G0/G1期。通过上调裂解型多磷酸腺苷核糖聚合酶、caspase-9、caspase-8、caspase-3和Bax, hdea处理的HT-29细胞发生凋亡,但抑制Bcl-2,破坏核形态和ΔΨm。此外,处理后的HT-29细胞通过上调轻链3-II和beclin-1发生自噬。最后,HDEA抑制PI3K、AKT和mTOR的表达。因此,HDEA通过调控PI3K/AKT/mTOR信号通路诱导HT-29细胞凋亡、自噬和细胞周期阻滞,对HT-29细胞具有抗癌作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Ethyl Acetate Extract of <i>Halymenia durvillei</i> Induced Apoptosis, Autophagy, and Cell Cycle Arrest in Colorectal Cancer Cells.

Ethyl Acetate Extract of <i>Halymenia durvillei</i> Induced Apoptosis, Autophagy, and Cell Cycle Arrest in Colorectal Cancer Cells.

Ethyl Acetate Extract of <i>Halymenia durvillei</i> Induced Apoptosis, Autophagy, and Cell Cycle Arrest in Colorectal Cancer Cells.

Ethyl Acetate Extract of Halymenia durvillei Induced Apoptosis, Autophagy, and Cell Cycle Arrest in Colorectal Cancer Cells.

Colorectal cancer is one of the most death-dealing cancers. However, conventional cancer treatments still have side effects. Therefore, novel chemotherapeutic agents with less side effects are still in search. A marine red seaweed, Halymenia durvillei, is recently interested in its anticancer effects. This study investigated the anticancer effect of ethyl acetate extract of H. durvillei (HDEA) on HT-29 colorectal cancer cells in association with the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway. HDEA-treated HT-29 and OUMS-36 cells were used for cell viability tests by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyltetrazolium bromide assay. The effects of HDEA on apoptosis and cell cycle were evaluated. The nuclear morphology and mitochondrial membrane potential (ΔΨm) were observed by Hoechst 33342 and JC-1 staining, respectively. The gene expression of PI3K, AKT, and mTOR genes was evaluated using a real-time semiquantitative reverse transcription-polymerase chain reaction. The corresponding protein expressions were assessed by western blot analysis. The result revealed that the cell viability of treated HT-29 cells diminished while that of OUMS-36 cells was non-significant. By the down-regulation of cyclin-dependent ki-nase 4 and cyclin D1, HDEA-treated HT-29 cells were arrested in the G0/G1 phase. By the up-regulation of cleaved poly(adenosine diphosphate-ribose) polymerase, caspase-9, caspase-8, caspase-3, and Bax, HDEA-treated HT-29 cells underwent apoptosis, but suppressed Bcl-2, disrupted nuclear morphology and ΔΨm. Furthermore, treated HT-29 cells underwent autophagy by up-regulation of light chain 3-II and beclin-1. Lastly, HDEA suppressed the expression of PI3K, AKT, and mTOR. Therefore, HDEA exerts anticancer effects against HT-29 cells, confirmed by apoptosis, autophagy, and cell cycle arrest induction via regulation of the PI3K/AKT/mTOR signaling pathway.

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来源期刊
Preventive Nutrition and Food Science
Preventive Nutrition and Food Science Agricultural and Biological Sciences-Food Science
CiteScore
3.40
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35
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