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首页> 外文期刊>Journal of experimental & clinical cancer research : >Dehydrodiisoeugenol inhibits colorectal cancer growth by endoplasmic reticulum stress-induced autophagic pathways
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Dehydrodiisoeugenol inhibits colorectal cancer growth by endoplasmic reticulum stress-induced autophagic pathways

机译：脱氢二异蛋烯醇通过内质网胁迫诱导的自噬途径抑制结肠直肠癌生长

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Dehydrodiisoeugenol (DEH), a novel lignan component extracted from nutmeg, which is the seed of Myristica fragrans Houtt, displays noticeable anti-inflammatory and anti-allergic effects in digestive system diseases. However, the mechanism of its anticancer activity in gastrointestinal cancer remains to be investigated. In this study, the anticancer effect of DEH on human colorectal cancer and its underlying mechanism were evaluated. Assays including MTT, EdU, Plate clone formation, Soft agar, Flow cytometry, Electron microscopy, Immunofluorescence and Western blotting were used in vitro. The CDX and PDX tumor xenograft models were used in vivo. Our findings indicated that treatment with DEH arrested the cell cycle of colorectal cancer cells at the G1/S phase, leading to significant inhibition in cell growth. Moreover, DEH induced strong cellular autophagy, which could be inhibited through autophagic inhibitors, with a rction in the DEH-induced inhibition of cell growth in colorectal cancer cells. Further analysis indicated that DEH also induced endoplasmic reticulum (ER) stress and subsequently stimulated autophagy through the activation of PERK/eIF2α and IRE1α/XBP-1?s/CHOP pathways. Knockdown of PERK or IRE1α significantly decreased DEH-induced autophagy and retrieved cell viability in cells treated with DEH. Furthermore, DEH also exhibited significant anticancer activities in the CDX- and PDX-models. Collectively, our studies strongly suggest that DEH might be a potential anticancer agent against colorectal cancer by activating ER stress-induced inhibition of autophagy.
机译：脱水脱苯酚（DEH），一种从肉豆蔻提取的新型木兰组分，即肌肌瘤Houtt的种子，在消化系统疾病中显示出明显的抗炎和抗过敏作用。然而，其胃肠癌中抗癌活性的机制仍有待研究。在这项研究中，评估了DEH对人结肠直肠癌及其潜在机制的抗癌作用。在体外使用包括MTT，EDU，板克隆形成，软琼脂，流式细胞术，电子显微镜，免疫荧光和Western印迹的测定。 CDX和PDX肿瘤异种移植模型用于体内。我们的研究结果表明，用DEH的治疗在G1 / S期内捕获结直肠癌细胞的细胞周期，导致细胞生长的显着抑制。此外，DEH诱导强细胞自噬，可以通过自噬抑制剂抑制，其在DEH诱导的细胞生长中抑制结肠直肠癌细胞中的抑制。进一步的分析表明，DEH还诱导内质网（ER）应激，随后通过激活Perk /EIF2α和IRE1α/ XbP-1αs/ Chop途径刺激自噬。 PERK或IS1α的敲低显着降低了DEH诱导的自噬和检索用DEH处理的细胞中的细胞活力。此外，DEH还在CDX和PDX模型中表现出显着的抗癌活动。统称，我们的研究强烈建议，通过激活ER应激诱导的自噬抑制，DEH可能是针对结肠直肠癌的潜在抗癌剂。

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