Lentiviral vector-mediated shRNA against AIMP2-DX2 suppresses lung cancer cell growth through blocking glucose uptake

Seung Hee Chang, Youn Sun Chung, Soon Kyung Hwang, Jung Taek Kwon, Arash Minai-Tehrani, Sunghoon Kim, Seung Bum Park, Yeon Soo Kim, Myung Haing Cho

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7 Citations (Scopus)

Abstract

Aminoacyl-tRNA synthetases [ARS]-interacting multifunctional protein 2 (AIMP2) has been implicated in the control of cell fate and lung cell differentiation. A variant of AIMP2 lacking exon 2 (AIMP2-DX2) is expressed in different cancer cells. We previously studied the expression level of AIMP2-DX2 in several lung cell lines and reported elevated expression levels of AIMP2-DX2 in NCI-H460 and NCI-H520. Here, we report that the suppression of AIMP2-DX2 by lentivirus mediated short hairpin (sh)RNA (sh-DX2) decreased the rate of glucose uptake and glucose transporters (Gluts) in NCI-H460 cells. Down-regulation of AIMP2-DX2 reduced glycosyltransferase (GnT)-V in the Golgi apparatus, while inducing the GnT-V antagonist GnT-III. Down-regulation of AIMP2-DX2 also suppressed the epidermal growth factor receptor/mitogen activated protein kinase (EGFR/MAPK) signaling pathway, leading to the decrease of the proliferation marker Ki-67 expression in nuclei. Furthermore, dual luciferase activity reduced cap-dependent protein translation in cells infected with sh-DX2. These results suggest that AIMP2-DX2 may be a relevant therapeutic target for lung cancer, and that the sh-DX2 lentiviral system can be an appropriate method for lung cancer therapy.

Original languageEnglish
Pages (from-to)553-562
Number of pages10
JournalMolecules and cells
Volume33
Issue number6
DOIs
Publication statusPublished - 2012 Jun 1

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Cell Biology

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    Chang, S. H., Chung, Y. S., Hwang, S. K., Kwon, J. T., Minai-Tehrani, A., Kim, S., Park, S. B., Kim, Y. S., & Cho, M. H. (2012). Lentiviral vector-mediated shRNA against AIMP2-DX2 suppresses lung cancer cell growth through blocking glucose uptake. Molecules and cells, 33(6), 553-562. https://doi.org/10.1007/s10059-012-2269-2