Canopy Homolog 2 contributes to liver oncogenesis by promoting unfolded protein response–dependent destabilization of tumor protein P53,Hepatology

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Canopy Homolog 2 contributes to liver oncogenesis by promoting unfolded protein response–dependent destabilization of tumor protein P53
Hepatology ( IF 12.9 ) Pub Date : 2022-01-05 , DOI: 10.1002/hep.32318
Feng Hong _{1,

2,

3} , Ching Ying Lin ₄ , Jingyue Yan ₅ , Yizhou Dong ₅ , Yuli Ouyang _{1,

2,

3} , Doyeon Kim _{1,

2,

3} , Xiaoli Zhang ₆ , Bei Liu ₇ , Shaoli Sun ₈ , Wei Gu ₉ , Zihai Li _{1,

2,

3}

Affiliation

Abnormalities in the tumor protein P53 (p53) gene and overexpression of mouse double minute 2 homolog (MDM2), a negative regulator of p53, are commonly observed in cancers. p53 destabilization is regulated by endoplasmic reticulum (ER) stress and unfolded protein response (UPR) in cancer. However, the mechanisms remain enigmatic. Canopy homolog 2 (CNPY2) is a key UPR initiator that primarily involved in ER stress and is highly expressed in the liver, but its functional role in regulating liver carcinogenesis is poorly understood. Therefore, we aimed to investigate the role of CNPY2 in hepartocarcinogenesis through URP-dependent p53 destabilization.

中文翻译：

Canopy Homolog 2 通过促进肿瘤蛋白 P53 的未折叠蛋白反应依赖性去稳定化促进肝癌发生

肿瘤蛋白 P53 ( p53 ) 基因的异常和小鼠双分钟 2 同系物 (MDM2)（p53 的负调节因子）的过度表达在癌症中很常见。p53 不稳定受癌症中内质网 (ER) 应激和未折叠蛋白反应 (UPR) 的调节。然而，这些机制仍然是个谜。Canopy 同系物 2 (CNPY2) 是一种关键的 UPR 引发剂，主要参与 ER 应激，并在肝脏中高表达，但其在调节肝癌发生中的功能作用知之甚少。因此，我们旨在通过 URP 依赖性 p53 去稳定化研究 CNPY2 在肝癌发生中的作用。

更新日期：2022-01-05

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