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首页> 外文期刊>Journal of cellular biochemistry. >Resistance to 3-HTMC-Induced Apoptosis Through Activation of PI3K/Akt, MEK/ERK, and p38/COX-2/PGE(2) Pathways in Human HT-29 and HCT116 Colorectal Cancer Cells
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Resistance to 3-HTMC-Induced Apoptosis Through Activation of PI3K/Akt, MEK/ERK, and p38/COX-2/PGE(2) Pathways in Human HT-29 and HCT116 Colorectal Cancer Cells

机译：通过PI3K / AKT，MEK / ERK和P38 / COX-2 / PGE（2）途径在人HT-29和HCT116结直肠癌细胞中激活抗3-HTMC诱导的细胞凋亡

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摘要

Increasing incidence and mortality of colorectal cancer brings the necessity to uncover new possibilities in its prevention and treatment. Chalcones have been identified as interesting compounds having chemopreventive and antitumor properties. In this study, we investigated the effects of the synthetic chalcone derivative 3-hydroxy-3,4,4,5-tetra-methoxy-chalcone (3-HTMC) on proliferation, cell cycle distribution, apoptosis, and its mechanism of action in human colorectal HT-29 (COX-2 sufficient) and HCT116 (COX-2 deficient) cancer cells. We showed that 3-HTMC decreased cell viability in a dose-dependent manner with a more potent antiproliferative effect on HCT116 than HT-29 cells. Flow cytometric analysis revealed G(2)/M cell cycle accumulation in HT-29 cells and significant G(2)/M arrest in HCT116 cells with a subsequent apoptosis shown by appearance of Sub-G1 peak. We demonstrated that 3-HTMC treatment on both cell lines induced apoptotic process associated with overexpression of death receptor DR5, activation of caspase-8 and -3, PARP cleavage, and DNA fragmentation. In addition, 3-HTMC induced activation of PI3K/Akt and MEK/ERK principal survival pathways which delay 3-HTMC-induced apoptosis in both cell lines. Furthermore, COX-2 overexpression in HT-29 cells contributes to apoptosis resistance which explains the difference of sensitivity between HT-29 and HCT116 cells to 3-HTMC treatment. Even if resistance mechanisms to apoptosis reduced chalcone antitumoral potential, our results suggest that 3-HTMC may be considered as an interesting compound for colorectal cancer therapy or chemoprevention. J. Cell. Biochem. 117: 2875-2885, 2016. (c) 2016 Wiley Periodicals, Inc.
机译：增加结直肠癌的发病率和死亡率使必要揭示预防和治疗中的新可能性。已鉴定为具有化学预防和抗肿瘤性质的有趣化合物的Chalcones。在这项研究中，我们研究了合成的硫酮衍生物3-羟基-3,4,5-甲氧基 - Chalcone（3-HTMC）对增殖，细胞周期分布，细胞凋亡及其作用机制的影响人结肠直肠HT-29（COX-2足以）和HCT116（COX-2不足）癌细胞。我们表明，3-HTMC以剂量依赖性方式降低了细胞活力，对HCT116比HT-29细胞更有效的抗增殖作用。流式细胞术分析显示HT-29细胞中的G（2）/ m细胞周期积累，并在HCT116细胞中抑制了HCT116细胞，随后通过子G1峰的出现所示。我们证明，对细胞系的3-HTMC处理诱导与死亡受体DR5的过表达相关的凋亡过程，激活Caspase-8和-3，PARP切割和DNA碎片。此外，3-HTMC诱导的PI3K / AKT和MEK / ERK主存活途径激活，其延迟了两种细胞系中的3-HTMC诱导的细胞凋亡。此外，HT-29细胞中的COX-2过表达有助于凋亡抗性，其解释了HT-29和HCT116细胞对3-HTMC处理之间的敏感性的差异。即使抗凋亡的抗性机制降低了醌抗肿瘤潜力，我们的结果表明，3-HTMC可以被认为是用于结直肠癌治疗或化学普查的有趣化合物。 J.Cell。生物学习。 117：2875-2885,2016。（c）2016年Wiley期刊，Inc。

著录项

  • 来源
    《Journal of cellular biochemistry.》 |2016年第12期|共11页
  • 作者

    Semaan Josiane; Pinon Aline; Rioux Benjamin; Hassan Lama; Limami Youness; Pouget Christelle; Fagnere Catherine; Sol Vincent; Diab-Assaf Mona; Simon Alain; Liagre Bertrand;

  • 作者单位

    Univ Limoges Lab Chem Nat Subst Fac Pharm FR GEIST 3503 EA1069 F-EA1069 Limoges France;

    Univ Limoges Lab Chem Nat Subst Fac Pharm FR GEIST 3503 EA1069 F-EA1069 Limoges France;

    Univ Limoges Lab Chem Nat Subst Fac Pharm FR GEIST 3503 EA1069 F-EA1069 Limoges France;

    Univ Limoges Lab Chem Nat Subst Fac Pharm FR GEIST 3503 EA1069 F-EA1069 Limoges France;

    Univ Mohammed VI Sci Sante LNR Casablanca Morocco;

    Univ Limoges Lab Chem Nat Subst Fac Pharm FR GEIST 3503 EA1069 F-EA1069 Limoges France;

    Univ Limoges Lab Chem Nat Subst Fac Pharm FR GEIST 3503 EA1069 F-EA1069 Limoges France;

    Univ Limoges Lab Chem Nat Subst Fac Pharm FR GEIST 3503 EA1069 F-EA1069 Limoges France;

    Lebanese Univ Mol Tumorigenesis &

    Anticanc Pharmacol EDST Hadath Lebanon;

    Univ Limoges Lab Chem Nat Subst Fac Pharm FR GEIST 3503 EA1069 F-EA1069 Limoges France;

    Univ Limoges Lab Chem Nat Subst Fac Pharm FR GEIST 3503 EA1069 F-EA1069 Limoges France;

  • 收录信息
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 生物化学;
  • 关键词

    3-HTMC; APOPTOSIS; COLORECTAL CANCER; PI3K; Akt; ERK; COX-2;

    机译：3-htmc;细胞凋亡;结直肠癌;pi3k;akt;erk;cox-2;

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