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LKB1 and YAP phosphorylation play important roles in Celastrol-induced β-catenin degradation in colorectal cancer
Therapeutic Advances in Medical Oncology ( IF 4.3 ) Pub Date : 2019-04-22 , DOI: 10.1177/1758835919843736
Shuren Wang 1 , Kai Ma 1 , Cuiqi Zhou 2 , Yu Wang 1 , Guanghui Hu 1 , Lechuang Chen 1 , Zhuo Li 3 , Chenfei Hu 1 , Qing Xu 1 , Hongxia Zhu 1 , Mei Liu 4 , Ningzhi Xu 5
Affiliation  

As the most common gastrointestinal (GI) tract cancer worldwide, colorectal cancer (CRC) represents the fifth leading causes of cancer deaths among both men and women.1 CRC acquires many genetic alterations, and some signaling pathways involved are clearly singled out as key factors in tumor formation. Activation of the Wnt pathway is regarded as the initiating event in CRC.2 The core of Wnt signaling is β-catenin, which is regulated by a cytoplasmic destruction complex consisting of a central scaffold protein Axin, adenomatous polyposis coli (APC), glycogen synthase kinase 3β (GSK-3β), and casein kinase 1 (CK1).3 As an critical transcriptional co-activator of the Wnt pathway, β-catenin regulates target gene expression.4 Aberrant expression of β-catenin induces malignant transformation of normal cells, and its abnormal activity has been reported in many cancer types.

中文翻译:

LKB1和YAP磷酸化在Celastrol诱导的大肠癌β-catenin降解中起重要作用

作为全球最常见的胃肠道癌,大肠癌(CRC)代表男性和女性中癌症死亡的第五大主要原因。1 CRC获得了许多遗传改变,并且涉及的某些信号传导途径被明确选出为肿瘤形成的关键因素。Wnt途径的激活被认为是CRC中的起始事件。2 Wnt信号转导的核心是β-catenin,其受细胞质破坏复合物调控,该复合物由中央支架蛋白Axin,腺瘤性息肉病(APC),糖原合酶激酶3β(GSK-3β)和酪蛋白激酶1(CK1)组成。 )。3作为Wnt途径的关键转录共激活因子,β-catenin调节靶基因的表达。4 β-catenin的异常表达诱导正常细胞的恶性转化,并且在许多癌症类型中均已报道其异常活性。
更新日期:2019-04-22
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