Investigation of chromatin remodeling by histone modifier protein in carcinogenesis and progression.

已经证明MEK-ERK 1/2-Elk-1通路导致EZH 2过表达。已知乳腺癌的三阴性和ERBB 2过表达亚型含有更快速增殖的乳腺癌细胞。与EZH 2过表达相关的信号通路与乳腺癌的两种侵袭性亚型相关，显示了组蛋白修饰蛋白过表达的临床病理学意义之一。EZH 2是一种由致癌突变型RAS诱导的组蛋白修饰蛋白，其致癌作用也在胰腺癌发生中被定义，使用外源表达人突变型RAS的转基因大鼠的胰腺癌。也就是说，发现EZH 2是胰腺癌发生中MEK-ERK通路下游的真实的效应蛋白。

It is demonstrated that MEK-ERK1/2-Elk-1 pathway leads to EZH2 overexpression. The triple-negative and ERBB2-overexpressing subtypes of breast cancer are known to contain more rapidly proliferating breast cancer cells. The signaling pathway connected to EZH2 overexpression was associated with both aggressive subtypes of breast cancer, showing one of the clinicopathological significance of overexpression of histone modifier protein. The oncogenic role of EZH2, a histone modifier protein that is induced by oncogenic mutant RAS is also defined in pancreatic carcinogenesis, using pancreatic cancers of transgenic rats exogenously expressing human mutant RAS. That is, EZH2 was found to be a real effecter protein in the downstream of the MEK-ERK pathway in pancreatic carcinogenesis.