KLF10，转化生长因子-β诱导早期基因 1，作为一种肿瘤抑制因子发挥作用。
KLF10, transforming growth factor-β-inducible early gene 1, acts as a tumor suppressor.
机构信息
Center for Agricultural Biomaterials, Seoul National University, Seoul 151-921, South Korea.
出版信息
Biochem Biophys Res Commun. 2012 Mar 9;419(2):388-94. doi: 10.1016/j.bbrc.2012.02.032. Epub 2012 Feb 13.
Krüppel-like factor 10 (KLF10) has been suggested to be a putative tumor suppressor. In the present study, we generated KLF10 deficient mice to explore this hypothesis in vivo. KLF10 deficient mice exhibited increased predisposition to skin tumorigenesis and markedly accelerated papilloma development after DMBA/TPA treatment. On the other hand, KLF10 deficient keratinocytes showed increased proliferation and apoptosis. In colony formation assays after oncogenic H-Ras transfection, KLF10 deficient mouse embryonic fibroblasts (MEFs) yielded more colonies than wild-type MEFs. Furthermore, KLF10 dose-dependently activated p21(WAF1/CIP1) transcription, which was independent of p53 and Sp1 binding sites in p21(WAF1/CIP1) promoter. This study demonstrates that KLF10 is a tumor suppressor and that it targets p21(WAF1/CIP1) transcription.
Krüppel 样因子 10（KLF10）被认为是一种潜在的肿瘤抑制因子。在本研究中，我们生成了 KLF10 缺陷型小鼠，以在体内探索这一假说。KLF10 缺陷型小鼠表现出增加的皮肤肿瘤易感性，并在 DMBA/TPA 处理后明显加速了乳头瘤的发展。另一方面，KLF10 缺陷型角质形成细胞表现出增加的增殖和凋亡。在致癌 H-Ras 转染后的集落形成实验中，KLF10 缺陷型小鼠胚胎成纤维细胞（MEFs）比野生型 MEFs 产生更多的集落。此外，KLF10 剂量依赖性地激活了 p21（WAF1/CIP1）转录，这与 p21（WAF1/CIP1）启动子中的 p53 和 Sp1 结合位点无关。这项研究表明，KLF10 是一种肿瘤抑制因子，它靶向 p21（WAF1/CIP1）转录。
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