首页> 外文期刊>Journal of Biology and Life Science >Knock-Down of Id1 and Id3 Proteins Induces Apoptosis in Human Colon Carcinoma (HCT116) Cells
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Knock-Down of Id1 and Id3 Proteins Induces Apoptosis in Human Colon Carcinoma (HCT116) Cells

机译:击倒Id1和Id3蛋白诱导人结肠癌(HCT116)细胞凋亡

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Id (Inhibitor of differentiation) proteins belong to the Helix-Loop-Helix (HLH) group of transcription factors and they are characterized by the absence of their DNA-binding domain. Id proteins are involved in cellular processes. These biological roles include cell growth, differentiation, senescence, apoptosis, angiogenesis and neoplastic transformation. This work aimed at investigating the consequences of down-regulating Id proteins on growth and pro-apoptotic functions in an in vitro model using HCT116 by siRNA gene knock-down. This objective was achieved by using antisense oligonucleotides complementary to Id1, Id2 and Id3 mRNA on human epithelial colon carcinoma cell line (HCT116). Silencing of Id1 and Id3 in HCT116 resulted in widespread cell death but not S-phase arrest. Interestingly, knock-down of Id2 neither resulted in induction of apoptosis nor cell growth arrest. However, since it was able to reduce viable cell populations of HCT116 at 48 h post-transfection, it may imply that cell death and growth arrest following down-regulation of Id2 may occur via a different mechanism. These observations suggest that Id1 and Id3 could provide some therapeutic opportunities to cure colonic cancers.?
机译:Id(分化抑制剂)蛋白属于转录因子的螺旋-螺旋-螺旋(HLH)组,其特征是不存在其DNA结合结构域。 Id蛋白参与细胞过程。这些生物学作用包括细胞生长,分化,衰老,凋亡,血管生成和肿瘤转化。这项工作旨在研究通过siRNA基因敲低在体外模型中使用HCT116下调Id蛋白对生长和促凋亡功能的影响。通过使用与人上皮结肠癌细胞系(HCT116)上的Id1,Id2和Id3 mRNA互补的反义寡核苷酸来实现此目标。 HCT116中Id1和Id3的沉默导致广泛的细胞死亡,但未导致S期停滞。有趣的是,敲除Id2既不会诱导凋亡也不会导致细胞生长停滞。但是,由于它能够在转染后48小时减少HCT116的存活细胞群,因此可能暗示Id2下调后的细胞死亡和生长停滞可能是通过不同的机制发生的。这些观察结果表明,Id1和Id3可以提供一些治疗结肠癌的治疗机会。

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