SHP2与乳腺癌侵袭转移相关性的研究进展  被引量:1

Role of SHP2 in invasion and metastasis of breast cancer

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作  者:陈钦[1] 郑瑛[1] 张斌[1] 曹旭晨[1] 

机构地区:[1]天津医科大学肿瘤医院乳腺一科,国家肿瘤临床医学研究中心,天津市肿瘤防治重点实验室,乳腺癌防治教育部重点实验室,天津市300060

出  处:《中国肿瘤临床》2014年第15期999-1002,共4页Chinese Journal of Clinical Oncology

基  金:天津市自然科学基金项目(编号:11JCZDJC28000)资助~~

摘  要:含Src同源区2蛋白质酪氨酸磷酸酶(Src homology 2 domain containing protein tyrosine phosphatases,SHP2)是一种跨膜型蛋白酪氨酸磷酸酶,通过调节细胞内蛋白质的酪氨酸磷酸化水平,在细胞信号转导通路及控制细胞活性中发挥重要的作用。其活化状态与乳腺癌发生发展过程中的Ras/ERK,PI3K/Akt/mTOR等信号通路、激素水平、侵袭转移、肿瘤干细胞的生物学行为等密切相关。SHP2基因的敲除或抑制SHP2蛋白表达,可不同程度阻断与乳腺癌侵袭、转移相关的信号通路,从而抑制肿瘤生长,甚至不可逆地使肿瘤丧失重新获得干细胞特性的能力。因此,SHP2很可能为抗肿瘤药物的研发提供一个新的靶点。本文就SHP2与乳腺癌侵袭转移的相关研究进展进行综述。Src homology 2 domain-containing phosphatase (SHP2), which is encoded by proto-oncogene PTPN11, is one of the transmembrane protein-tyrosine phosphatases. SHP2 has an important function in signal transduction pathways and activities of cells through the regulation of tyrosine phosphorylation level of intracellular proteins. The status of SHP2 activation is closely connected with the regulation of hormone levels, state of invasion and metastasis of tumor, development and progression of tumor stem cells of breast cancer, as well as signal pathways including Ras/ERK and PI3K/Akt/mTOR. Gene knockout or gene silencing expression helps inhibit tumor growth, irreversibly hindering the ability of the tumor to regain stem cells and disturb the signal pathways of the invasion and metastasis of breast cancer. Recent studies have shown that SHP2 may help in bringing anticancer drugs to a higher level. This article concentrates on the research progress in relationship of SHP2 with invasion and metastasis of breast cancer.

关 键 词:SHP2 信号通路 乳腺癌 转移 

分 类 号:R737.9[医药卫生—肿瘤]

 

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