Insights into significance of combined inhibition of MEK and m-TOR signalling output in KRAS mutant non-small-cell lung cancer

Br J Cancer. 2016 Aug 23;115(5):549-52. doi: 10.1038/bjc.2016.220. Epub 2016 Jul 21.

Abstract

Background: We aimed to understand the dependence of MEK and m-TOR inhibition in EGFR(WT)/ALK(non-rearranged) NSCLC cell lines.

Methods: In a panel of KRAS(M) and KRAS(WT) NSCLC cell lines, we determined growth inhibition (GI) following maximal reduction in p-ERK and p-S6RP caused by trametinib (MEK inhibitor) and AZD2014 (m-TOR inhibitor), respectively.

Results: GI caused by maximal m-TOR inhibition was significantly greater than GI caused by maximal MEK inhibition in the cell line panel (52% vs 18%, P<10(-4)). There was no significant difference in GI caused by maximal m-TOR compared with maximal m-TOR+MEK inhibition. However, GI caused by the combination was significantly greater in the KRAS(M) cell lines (79% vs 61%, P=0.017).

Conclusions: m-TOR inhibition was more critical to GI than MEK inhibition in EGFR(WT)/ALK(non-rearranged) NSCLC cells. The combination of MEK and m-TOR inhibition was most effective in KRAS(M) cells.

MeSH terms

  • Carcinoma, Non-Small-Cell Lung / genetics
  • Carcinoma, Non-Small-Cell Lung / metabolism*
  • Cell Line, Tumor
  • Genes, ras*
  • Humans
  • Lung Neoplasms / genetics
  • Lung Neoplasms / metabolism*
  • MAP Kinase Kinase Kinases / metabolism*
  • Signal Transduction*
  • TOR Serine-Threonine Kinases / metabolism*

Substances

  • MTOR protein, human
  • TOR Serine-Threonine Kinases
  • MAP Kinase Kinase Kinases