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首页> 外文期刊>Cell biology international. >Extracellular‐signal‐regulated kinase/mitogen‐activated protein kinase signaling as a target for cancer therapy: an updated review
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Extracellular‐signal‐regulated kinase/mitogen‐activated protein kinase signaling as a target for cancer therapy: an updated review

机译：细胞外信号调节激酶/丝裂原蛋白激活蛋白激酶信号作为癌症治疗靶标：更新的审查

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Abstract Mitogen‐activated protein kinase (MAPK) signaling pathway is activated in a wide spectrum of human tumors, exhibiting cardinal oncogenic roles and sustained inhibition of this pathway is considered as a primary goal in clinic. Within this pathway, receptor tyrosine kinases such as epithelial growth factor receptor, mesenchymal–epithelial transition, and AXL act as upstream regulators of RAS/RAF/MEK/extracellular‐signal‐regulated kinase. MAPK signaling is active in both early and advanced stages of tumorigenesis, and it promotes tumor proliferation, survival, and metastasis. MAPK regulatory effects on cellular constituent of the tumor microenvironment is for immunosuppressive purposes. Cross‐talking between MAPK with oncogenic signaling pathways including WNT, cyclooxygenase‐2, transforming growth factor‐β, NOTCH and (in particular) with phosphatidylinositol 3‐kinase is contributed to the multiplication of tumor progression and drug resistance. Developing resistance (intrinsic or acquired) to MAPK‐targeted therapy also occurs due to heterogeneity of tumors along with mutations and negative feedback loop of interactions exist between various kinases causing rebound activation of this signaling. Multidrug regimen is a preferred therapeutic avenue for targeting MAPK signaling. To enhance patient tolerance and to mitigate potential adversarial effects related to the combination therapy, determination of a desired dose and drug along with pre‐evaluation of cancer‐type‐specific kinase mutation and sensitivity, especially for patients receiving triplet therapy is an urgent need.
机译：摘要丝裂原激活的蛋白激酶（MAPK）信号传导途径被激活在宽的人肿瘤中，表现出主要的致癌作用，并且对该途径的持续抑制被认为是临床的主要目标。在该途径内，受体酪氨酸激酶如上皮生长因子受体，间充心上皮过渡和AXL作为RAS / RAF / MEK /细胞外信号调节激酶的上游调节剂。 MAPK信令在肿瘤发生的早期和高级阶段都活跃，促进肿瘤增殖，生存和转移。 MAPK对肿瘤微环境细胞成分的MAPK调节效果用于免疫抑制目的。用WNT，环氧化酶-2，转化生长因子-2，与磷脂酰肌醇3-激酶的转化生长因子-2，凹口和（特别是）的雌激素信号传导途径之间的交叉谈话有助于肿瘤进展和耐药性的倍增。由于肿瘤的异质性以及突变和负反馈回路存在相互作用之间存在的各种激酶之间的突变和负反馈回路的产生抗性也发生了显影性（内在或获得的），导致该信号传导的反弹激活相互作用。 Multidrug方案是用于定位MAPK信号的首选治疗途径。为了增强患者耐受性并减轻与联合治疗相关的潜在的对抗效果，确定所需剂量和药物以及预评估癌型特异性激酶突变和敏感性，特别是对于接受三联疗法的患者是迫切需要的。

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