Hui Lijian, Bakiri Latifa, Stepniak Ewa, Wagner Erwin F
Research Institute of Molecular Pathology, Vienna, Austria.
Cell Cycle. 2007 Oct 15;6(20):2429-33. doi: 10.4161/cc.6.20.4774. Epub 2007 Oct 21.
The mitogen-activated protein kinase (MAPK) p38alpha is involved in numerous biological processes and is a drug target for inflammation-associated diseases. Genetic analysis in mice demonstrated that fetuses lacking p38alpha are embryonic lethal owing to impaired placental development. The function of p38alpha in mice after birth remained unclear until conditional alleles of p38alpha were used. It was found that p38alpha is essential for lung function in both neonatal and adult mice. Increased proliferation and impaired differentiation are the hallmarks of p38alpha-deficient cells. Moreover, mice deficient in p38alpha are prone to cancer development using carcinogen or oncogene-induced cancer models. p38alpha can suppress cell proliferation by antagonizing the JNK/c-Jun pathway, which is an important regulator of proliferation and apoptosis. These findings suggest that therapeutic inhibition of p38 might lead to unwanted proliferation. Therefore, a combined inhibition of p38 and other pathways, such as the JNK pathway, should be considered for targeting cancer inflammation.
丝裂原活化蛋白激酶(MAPK)p38α参与众多生物学过程,是炎症相关疾病的药物靶点。对小鼠的基因分析表明,缺乏p38α的胎儿由于胎盘发育受损而胚胎致死。在使用p38α的条件性等位基因之前,p38α在小鼠出生后的功能尚不清楚。研究发现,p38α对新生小鼠和成年小鼠的肺功能都至关重要。增殖增加和分化受损是p38α缺陷细胞的特征。此外,使用致癌物或致癌基因诱导的癌症模型时,缺乏p38α的小鼠易于发生癌症。p38α可通过拮抗JNK/c-Jun途径来抑制细胞增殖,而JNK/c-Jun途径是增殖和凋亡的重要调节因子。这些发现表明,对p38的治疗性抑制可能会导致不必要的细胞增殖。因此,针对癌症炎症,应考虑联合抑制p38和其他途径,如JNK途径。