p38丝裂原活化蛋白激酶通路在恶性脑肿瘤中的功能作用。
The functional role of p38 MAPK pathway in malignant brain tumors.
作者信息
Grave Nathália, Scheffel Thamiris Becker, Cruz Fernanda Fernandes, Rockenbach Liliana, Goettert Márcia Inês, Laufer Stefan, Morrone Fernanda Bueno
机构信息
Programa de Pós-Graduação em Medicina e Ciências da Saúde, Escola de Medicina, Pontifícia Universidade Católica do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil.
Laboratório de Farmacologia Aplicada, Escola de Ciências da Saúde e da Vida, Pontifícia Universidade Católica do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil.
出版信息
Front Pharmacol. 2022 Oct 3;13:975197. doi: 10.3389/fphar.2022.975197. eCollection 2022.
Gliomas are extremely debilitating malignant brain tumors with very limited response to therapies. The initiation and progression of gliomas can be attributed to several molecular abnormalities, such as mutations in important regulatory networks. In this regard, the mitogen-activated protein kinases (MAPKs) arise as key signaling pathways involved in cell proliferation, survival, and differentiation. MAPK pathway has been altered in most glial tumors. In glioma cells, the activation of p38 MAPK contributes to tumor invasion and metastasis and is positively correlated with tumor grade, being considered a potential oncogenic factor contributing to brain tumorigenesis and chemotherapy resistance. Hence, a better understanding of glioma pathogenesis is essential to the advancement of therapies that provide extended life expectancy for glioma patients. This review aims to explore the role of the p38 MAPK pathway in the genesis and progression of malignant brain tumors.
胶质瘤是极具破坏性的恶性脑肿瘤，对治疗的反应非常有限。胶质瘤的发生和进展可归因于多种分子异常，例如重要调控网络中的突变。在这方面，丝裂原活化蛋白激酶（MAPK）作为参与细胞增殖、存活和分化的关键信号通路而出现。MAPK通路在大多数胶质瘤中发生了改变。在胶质瘤细胞中，p38 MAPK的激活有助于肿瘤侵袭和转移，并且与肿瘤分级呈正相关，被认为是导致脑肿瘤发生和化疗耐药的潜在致癌因素。因此，更好地理解胶质瘤发病机制对于开发能够延长胶质瘤患者预期寿命的治疗方法至关重要。本综述旨在探讨p38 MAPK通路在恶性脑肿瘤发生和进展中的作用。
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