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首页> 外文期刊>Cancer Cell >NCOA5 Haploinsufficiency Results in Glucose Intolerance and Subsequent Hepatocellular Carcinoma
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NCOA5 Haploinsufficiency Results in Glucose Intolerance and Subsequent Hepatocellular Carcinoma

机译：NCOA5单倍剂量不足导致葡萄糖耐受不良和随后的肝细胞癌

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摘要

Type 2 diabetes (T2D) and male gender are associated with hepatocellular carcinoma (HCC) development. We demonstrate that heterozygous deletion of the Ncoa5 gene causes spontaneous development of HCC exclusively in male mice. Tumor development is preceded by increased interleukin-6 (IL-6) expression, early-onset glucose intolerance, and progressive steatosis and dysplasia in livers. Blockading IL-6 overexpression averts glucose intolerance and partially deters HCC development. Moreover, reduced NCOA5 expression is associated with a fraction of human HCCs and HCCs with comorbid T2D. These findings suggest that NCOA5 is a haploinsufficient tumor suppressor and that NCOA5 deficiency increases susceptibility to both glucose intolerance and HCC, partially by increasing IL-6 expression. Thus, our findings open additional avenues for developing therapeutic approaches to combat these diseases.
机译：2型糖尿病（T2D）和男性与肝细胞癌（HCC）的发展有关。我们证明，Ncoa5基因的杂合性缺失仅在雄性小鼠中引起HCC的自发发展。在肿瘤发展之前，白细胞介素6（IL-6）的表达增加，早期发作的葡萄糖耐受不良以及肝脏进行性脂肪变性和发育异常。阻断IL-6的过度表达可避免葡萄糖耐受不良并部分阻止HCC的发展。此外，降低的NCOA5表达与部分人类HCC和合并T2D的HCC相关。这些发现表明NCOA5是单倍体不足的肿瘤抑制剂，并且NCOA5缺乏通过部分增加IL-6表达而增加了对葡萄糖耐量和HCC的敏感性。因此，我们的发现为开发抗击这些疾病的治疗方法开辟了其他途径。

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