Krüppel-like factor 17, a novel tumor suppressor: its low expression is involved in cancer metastasis.
Krüppel-like factor 17, a novel tumor suppressor: its low expression is involved in cancer metastasis.
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新型抑癌因子Kruppel样因子17：其低表达参与癌症转移
DOI：
10.1007/s13277-015-4588-3
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发表时间：
2016-02
期刊：
影响因子：
--
通讯作者：
Tang F
中科院分区：
文献类型：
--
作者：
Zhou S;Tang X;Tang F
Krüppel样因子（KLF）家族是高度保守的锌指转录因子，参与调控细胞增殖、分化、凋亡和迁移。KLF 17是KLF家族的成员。最近的研究表明，KLF 17在人类肿瘤中的低表达和失活是由microRNA、基因突变和杂合性丢失引起的，参与了肿瘤的进展。KLF 17低表达增加了肿瘤的转移活力，其机制是通过调节上皮间质转化（EMT）相关基因的表达，介导EMT的发生; KLF 17低表达还通过上调DNA结合抑制因子1（ID 1）的表达，增加了肿瘤的转移。此外，突变型p53蛋白能够与KLF 17形成复合物，其介导KLF 17的消耗，抑制EMT基因转录并增加癌症转移。KLF 17的下调也介导了TGF-β通路的激活。
Krüppel-like factor (KLF) family is highly conserved zinc finger transcription factors that regulate cell proliferation, differentiation, apoptosis, and migration. KLF17 is a member of the KLF family. Recent studies have demonstrated that KLF17 low expression and inactivation are caused by microRNA, gene mutation, and loss of heterozygosity in human tumors, which participates in tumor progression. KLF17 low expression increases cancer metastatic viability; its mechanism is that low KLF17 mediates epithelial-mesenchymal transition (EMT) through regulating EMT-related genes expression; the reduced-KLF17 also increases cancer metastasis though upregulating inhibitor of DNA binding 1 (ID1). Additionally, mutant p53 proteins are capable of developing a complex with KLF17, which mediate the depletion of KLF17 inhibiting EMT gene transcription and increases cancer metastasis. KLF17 downregulation also mediates the activation of TGF-β pathway.