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Epithelial Mesenchymal Transition in Aggressive Lung Cancers

机译:腐蚀性肺癌中的上皮间充质转换

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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.
机译:癌细胞进入转移实体的进展有助于超过90%的癌症相关死亡。因此,转移的预防和治疗是一种未满足的临床需求。上皮到间充质转换(EMT)是一种进化保守的发育方案,其在癌症进展期间诱导并有助于转移性定植。 EMT通过增强迁移率,侵袭和对凋亡刺激抗性癌细胞赋予癌细胞的转移性。此外,EMT衍生的肿瘤细胞获得干细胞性能并表现出治疗性。提出募集到远处器官的播散肿瘤细胞随后通过间充质转换至上皮过渡(MET),高效定植和宏观塑料所需的EMT逆转。癌症研究的主要焦点是确定肿瘤侵袭,传播和转移中的EMT /满足的细胞和分子机制。在本章中,我们将专注于EMT信号通路在肺癌进展,癌症干细胞和获得EGFR酪氨酸激酶抑制剂和化疗的抗性的贡献。我们还将讨论以靶向EMT途径作为治疗肺癌的有吸引力策略的潜力。

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