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

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

Abstract

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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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。
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。
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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
自引率
0.00%
发文量
35
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