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首页> 外文期刊>Genes to cells : >FEAT enhances INSL3 expression in testicular Leydig cells
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FEAT enhances INSL3 expression in testicular Leydig cells

机译：emeg增强睾丸LEYDIG细胞中的INSL3表达

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摘要

FEAT, the protein encoded by methyltransferase-like 13 (METTL13), is aberrantly upregulated in most human cancers and potently drives tumorigenesis in vivo; however, its role in normal tissues remains elusive. Immunoblotting has displayed weak FEAT expression in normal human tissues, including the testis. Here, we found that FEAT is expressed in fetal and adult Leydig cells in the testis. FEAT knockdown using siRNA increased primary cilia formation in MA-10 Leydig tumor cells, accompanied by enhanced 5 ' adenosine monophosphate-activated protein kinase (AMPK) activation. Immunofluorescence analyses of FEAT-silenced MA-10 cells showed diminished insulin-like factor 3 (INSL3) expression. A male Mettl13(+/-) mouse developed bilateral intraabdominal cryptorchidism, suggesting defective INSL3 production by fetal Leydig cells. Leydig cells from the mouse showed markedly decreased INSL3 protein by immunohistochemistry. Together, these results suggest that FEAT facilitates the INSL3 production in testicular Leydig cells that is essential for transabdominal testis migration.
机译：Feat，由甲基转移酶样13（MetT113）编码的蛋白质在大多数人类癌症中异常上调，并且在体内有效地驱动肿瘤术;然而，它在正常组织中的作用仍然是难以捉摸的。免疫印迹在正常人体组织中显示出弱壮举，包括睾丸。在这里，我们发现壮举在睾丸中以胎儿和成人leydig细胞表达。使用siRNA的劣质敲低，在MA-10 leydig肿瘤细胞中增加原发性纤毛组，伴随着增强的5'腺苷一磷酸活性蛋白激酶（AMPK）活化。壮举的MA-10细胞的免疫荧光分析显示胰岛素样因子3（INSL3）表达的减少。雄性MetT11113（+/-）小鼠开发了双侧腹腔肾上腺晶状体，表明胎儿Leydig细胞的Insl3缺陷。来自小鼠的Leydig细胞显示通过免疫组织化学显着降低了INSL3蛋白质。这些结果表明，壮举促进了睾丸LEYDIG细胞中的INSL3生产，这对于跨境睾丸迁移至关重要。

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  • 来源
    《Genes to cells :》 |2018年第11期|共11页
  • 作者

    Li Yan; Kobayashi Kyosuke; Murayama Kosho; Kawahara Kohichi; Shima Yuichi; Suzuki Akira; Tani Kenzaburo; Takahashi Atsushi;

  • 作者单位

    Kyoto Univ Grad Sch Med Dept Hematol &

    Oncol Kyoto Japan;

    Kyushu Univ Med Inst Bioregulat Div Mol &

    Clin Genet Fukuoka Fukuoka Japan;

    Kyushu Univ Med Inst Bioregulat Div Mol &

    Clin Genet Fukuoka Fukuoka Japan;

    Kyushu Univ Med Inst Bioregulat Div Canc Genet Fukuoka Fukuoka Japan;

    Kawasaki Med Univ Dept Anat Kurashiki Okayama Japan;

    Kyushu Univ Med Inst Bioregulat Div Canc Genet Fukuoka Fukuoka Japan;

    Kyushu Univ Med Inst Bioregulat Div Mol &

    Clin Genet Fukuoka Fukuoka Japan;

    Kyoto Univ Grad Sch Med Dept Hematol &

    Oncol Kyoto Japan;

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  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 医学遗传学;
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