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Novel Therapeutics for Inhibiting Tumor Epithelial-Mesenchymal Transition (EMT), a Key Driver of Metastasis and a Mechanism of Drug-Resistance

机译:抑制肿瘤上皮 - 间充质转换(EMT),转移的关键驱动器和抗药性机制的新型治疗剂

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Epithelial-mesenchymal transition (EMT) plays a vital role in initiation of metastasis for cancer progression. It involves loss of epithelial characteristics and gain of features found in cells of mesenchymal and fibroblastic origin. Axl is a member of the TAM (Tyro3, Axl and Mer) family of receptor tyrosine kinases that has been shown to be upregulated by EMT inducers in breast cancer. In addition, role of Axl in EMT has been associated with resistance to EGFR and PI3K inhibitors, such as erlotinib in non-small cell lung cancer (NSCLC). In addition, Axl expression is associated with poor outcome in a wide variety of cancers including glioblastoma, prostate cancer, esophageal adenocarcinoma, pancreatic ductal adenocarcinoma (PDA), renal cell carcinoma, AML and CML.
机译:上皮 - 间充质转换(EMT)在癌症进展的转移中起着至关重要的作用。它涉及在间充质和纤维束起源细胞中发现的上皮特征和特征的增益。 AXL是TAM(Tyro3,AXL和MER)受体酪氨酸激酶系列的成员,其已被证明通过EMT诱导剂在乳腺癌中上调。此外,AXL在EMT中的作用已经与EGFR和PI3K抑制剂的抵抗有关,例如非小细胞肺癌(NSCLC)中的Erlotinib。此外,AXL表达与各种癌症的差异有关,包括胶质母细胞瘤,前列腺癌,食管腺癌,胰腺导管腺癌(PDA),肾细胞癌,AML和CML。

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