CDKs、Ras-ERK和PI3K-Aktin信号异常与癌症的探讨

S. Nandi, M. C. Bagchi
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引用次数: 2

摘要

癌症或恶性肿瘤可以定义为异常生长和细胞分裂。恶性肿瘤通过转移侵袭或植入远处,癌症细胞可以通过血液或淋巴系统转移到远处。体细胞遵循有丝分裂细胞的过程。正常细胞分裂通过负责细胞增殖和分化的原癌基因进行正常信号转导。这些原癌基因的突变导致癌基因通过异常信号转导改变基因表达和功能,使细胞生长失控。有丝分裂细胞周期由细胞周期蛋白依赖性激酶(CDKs)、Ras-ERK和PI3K-Akt的信号转导调节。异常信号通过这些基因的突变而发生,从而导致癌症。本综述简要报道了这些蛋白在异常信号传导和癌症中的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Exploring CDKs, Ras-ERK, and PI3K-Aktin Abnormal Signaling and Cancer
Cancer or malignancy can be defined as abnormal growth and cell division. Malignancies spread, through metastasis invasion, or implantation into distant sites by which cancer cells can move through the bloodstream or lymphatic system to distant locations. The body cells follow mitotic cell division process. Normal cell division occurs through the normal signal transduction through proto-oncogenes responsible for the cell proliferation and differentiation. Mutation of these proto-oncogene leads to oncogene which can modify the gene expression and function through abnormal signal transduction, making uncontrolled growth of cells. The mitotic cell cycle is regulated by the signal transduction through the cyclin dependent kinases (CDKs), Ras-ERK and PI3K-Akt.Abnormal signaling occurs through the mutation of these genes leading to the cancer. The present review shortly reported the role of these proteins in abnormal signal transduction and cancer.
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