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自噬在EGFR-TKI类肿瘤靶向药物对肺癌的治疗和耐药中作用的研究进展

张其程 徐克

中国肺癌杂志2016,Vol.19Issue(9):607-614,8.
中国肺癌杂志2016,Vol.19Issue(9):607-614,8.DOI:10.3779/j.issn.1009-3419.2016.09.09

自噬在EGFR-TKI类肿瘤靶向药物对肺癌的治疗和耐药中作用的研究进展

Advances in the Research of Autophagy in EGFR-TKI Treatment and Resistance in Lung Cancer

张其程 1徐克1

作者信息

  • 1. 300052天津,天津医科大学总医院,天津市肺癌研究所,天津市肺癌转移与肿瘤微环境重点实验室
  • 折叠

摘要

Abstract

Epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) is a group of targeted-drugs which effectively inhibits the growth of tumor cells with sensitive mutations inEGFR. However, the innate and acquired resis-tance are major obstacles of the effciency. Autophagy is a highly conserved self-digesting process in cells, which is considered to be associated with cancer development andchemoresistance. hTe activation of EGFR may regulate autophagy through mul-tiple signal pathways. EGFR-TKIs can induce autophagy, however, the function of the inducted autophagy remains biphasic. On one hand, autophagy induced by EGFR-TKI acts as a cytoprotective response in cancer cells, and autophagy inhibitors can enhance the cytotoxic effects of EGFR-TKI. On the other hand, a high level of autophagy atfer treatment of EGFR-TKI can also result in autophagic cell death lacking features of apoptosis, and the combination of EGFR-TKI with autophagy inducer might be beneifcial. hTus, autophagy regulation represents a promising approach for improving the effciency of EGFR-TKI in the treatment of cancer patients. Here we summarized the signaling pathways involved in EGFR-TKI induced autophagy, and reviewed the roles of autophagy in the treatment and chemoresistance of EGFR-TKI treatment in lung cancer.

关键词

表皮生长因子受体激酶抑制剂/自噬/耐药性/肺肿瘤

Key words

Epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI)/Autophagy/Drug resistance/Lung neoplasms

引用本文复制引用

张其程,徐克..自噬在EGFR-TKI类肿瘤靶向药物对肺癌的治疗和耐药中作用的研究进展[J].中国肺癌杂志,2016,19(9):607-614,8.

中国肺癌杂志

OA北大核心CSCDCSTPCDMEDLINE

1009-3419

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