Epithelial Mesenchymal Transition in Aggressive Lung Cancers
Epithelial Mesenchymal Transition in Aggressive Lung Cancers
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DOI：
10.1007/978-3-319-24932-2_3
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发表时间：
2016-01-01
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影响因子：
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通讯作者：
Mittal, Vivek
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文献类型：
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作者：
Mittal, Vivek
癌细胞进展为转移性实体导致超过90%的癌症相关死亡。因此，预防和治疗转移是一个未满足的临床需求。上皮间质转化（EMT）是一个进化保守的发育程序，在癌症进展过程中诱导并有助于转移定植。EMT通过增强迁移性、侵袭性和对凋亡刺激的抗性赋予癌细胞转移特性。此外，EMT衍生的肿瘤细胞获得干细胞特性并表现出治疗耐药性。被募集到远处器官的播散性肿瘤细胞随后通过间充质向上皮转化（MET）经历EMT逆转，这是有效定植和大转移所必需的。肿瘤研究的一个主要焦点是确定EMT/MET在肿瘤侵袭、扩散和转移中的细胞和分子机制。在本章中，我们将重点介绍EMT信号通路在肺癌进展、癌症干细胞和EGFR酪氨酸激酶抑制剂获得性耐药以及化疗中的作用。我们还将讨论靶向EMT通路作为治疗肺癌的有吸引力的策略的潜力。
The progression of a cancer cell into a metastatic entity contributes to more than 90 % of cancer related deaths. Therefore, the prevention and treatment of metastasis is an unmet clinical need. Epithelial to mesenchymal transition (EMT) is an evolutionary conserved developmental program, which is induced during cancer progression and contributes to metastatic colonization. EMT endows metastatic properties upon cancer cells by enhancing mobility, invasion, and resistance to apoptotic stimuli. Furthermore, EMT-derived tumor cells acquire stem cell properties and exhibit therapeutic resistance. The disseminated tumor cells recruited to distant organs are suggested to subsequently undergo an EMT reversion through mesenchymal to epithelial transition (MET), necessary for efficient colonization and macrometastasis. A major focus of cancer research is to determine the cellular and molecular mechanisms underlying EMT/MET in tumor invasion, dissemination and metastasis. In this chapter, we will focus on the contribution of the EMT signaling pathways in lung cancer progression, cancer stem cells and acquired resistance to EGFR tyrosine kinase inhibitors and chemotherapy. We will also discuss the potential of targeting EMT pathways as an attractive strategy for the treatment of lung cancer.