2. Academic Validation
  3. Inhibition of Mer and Axl receptor tyrosine kinases leads to increased apoptosis and improved chemosensitivity in human neuroblastoma

Inhibition of Mer and Axl receptor tyrosine kinases leads to increased apoptosis and improved chemosensitivity in human neuroblastoma

  • Biochem Biophys Res Commun. 2015 Feb 13;457(3):461-6. doi: 10.1016/j.bbrc.2015.01.017.
Yixin Li 1,  Xiqian Wang 2,  Shaojie Bi 3,  Kun Zhao 4,  Chao Yu 5
Affiliations

Affiliations

  • 1 Department of Medical Imaging, The Second Hospital of Shandong University, Jinan 250033, China. Electronic address: [email protected].
  • 2 Department of Orthopedic Surgery, The Second Hospital of Shandong University, Jinan 250033, China.
  • 3 Department of Cardiology, The Second Hospital of Shandong University, Jinan 250033, China.
  • 4 Department of Medical Imaging, The Second Hospital of Shandong University, Jinan 250033, China.
  • 5 Department of Clinical Laboratory, The Second Hospital of Shandong University, Jinan 250033, China.
PMID: 25596315 DOI: 10.1016/j.bbrc.2015.01.017
Abstract

Ectopic expression of Mer and Axl Receptor Tyrosine Kinases (RTKs) are frequently found in various cancers as known to promote oncogenesis by activating antiapoptotic signaling pathways. However, the roles of these receptors in neuroblastoma remain unclear. We found Mer and Axl was co-expressed in neuroblastoma patient samples and cell lines. Ligand-dependent Mer or Axl activation led to an increase in phosphorylated ERK1/2, Akt and FAK indicating roles for these RTKs in multiple oncogenic processes. Furthermore, Mer and Axl knockdown led to Apoptosis and inhibition of migration as well as a significant increase in chemosensitivity in response to cisplatin and vincristine treatment. Taken together, our results demonstrated that inhibition of Mer and Axl improved apoptotic response and chemosensitivity in neuroblastoma, providing new insights into development of novel therapeutic strategies by targeting these oncogenes.

Keywords

Axl; Chemosensitivity; Mer; Receptor tyrosine kinase; Targeted therapy.

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