Prostate-specific Klf6 Inactivation Impairs Anterior Prostate Branching Morphogenesis through Increased Activation of the Shh Pathway
Prostate-specific Klf6 Inactivation Impairs Anterior Prostate Branching Morphogenesis through Increased Activation of the Shh Pathway
复制标题
DOI：
10.1074/jbc.m109.001776
复制
发表时间：
2009-07-31
影响因子：
4.8
通讯作者：
Gao, Wei-Qiang
中科院分区：
文献类型：
--
作者：
Leow, Ching Ching;Wang, Bu-er;Gao, Wei-Qiang
Kruppel样因子6（Klf6）属于已知在发育和肿瘤抑制中起作用的锌指转录因子家族。尽管Klf6在前列腺癌中高度突变，但其在前列腺发育中的功能尚不清楚。我们已经产生了一个前列腺特异性Klf6缺陷的小鼠模型，并在这里报告一个新的作用Klf6在前列腺分支形态发生的调节。重要的是，我们的研究揭示了Klf6和Shh通路之间的新关系。Klf6缺陷导致刺猬途径组分（Shh、Ptc和Gli）水平升高以及它们的局部表达丧失，这反过来又导致侧向分支受损。
Kruppel-like factor 6 (Klf6) belongs to a family of zinc finger transcription factors known to play a role in development and tumor suppression. Although Klf6 is highly mutated in prostate cancer, its function in prostate development is unknown. We have generated a prostate-specific Klf6-deficient mouse model and report here a novel role for Klf6 in the regulation of prostate branching morphogenesis. Importantly, our study reveals a novel relationship between Klf6 and the Shh pathway. Klf6-deficiency leads to elevated levels of hedgehog pathway components (Shh, Ptc, and Gli) and loss of their localized expression, which in turn causes impaired lateral branching.