A pivotal role for Pim-1 kinase in esophageal squamous cell carcinoma involving cell apoptosis induced by reducing Akt phosphorylation

Oncol Rep. 2010 Oct;24(4):997-1004.

Abstract

It is well documented that Provirus integration site for Moloney murine leukemia virus 1 (Pim-1), as a proto-oncogene encoding a serine/threonine kinase with multiple cellular functions, is tightly associated with the occurrence and development of tumors. Overexpression of Pim-1 plays a critical role in the progression of several different tumors. In this study, esophageal squamous cell carcinoma (ESCC) EC9706 cells with Pim-1 siRNA treatment resulted in a clear decrease of Pim-1 levels, followed by inhibiting cell proliferation and inducing apoptosis. Further, Pim-1 siRNA reduced phosphorylation of Akt and Bad, and increased cleaved caspase-3/-9 activities and expression levels. These data suggest that Pim-1 siRNA-mediated apoptosis is closely related to the decrease in Akt and Bad phosphorylation and increase in cleaved caspase-3/-9 activities, and thus manipulation of Pim-1 is a potential target for molecular therapy in the clinical treatment of patients with ESCC.

MeSH terms

  • Apoptosis / physiology*
  • Blotting, Western
  • Carcinoma, Squamous Cell / enzymology*
  • Carcinoma, Squamous Cell / pathology
  • Cell Line, Tumor
  • Cell Separation
  • Esophageal Neoplasms / enzymology*
  • Esophageal Neoplasms / pathology
  • Flow Cytometry
  • Humans
  • Immunohistochemistry
  • Phosphorylation
  • Proto-Oncogene Mas
  • Proto-Oncogene Proteins c-akt / metabolism*
  • Proto-Oncogene Proteins c-pim-1 / metabolism*
  • RNA, Small Interfering
  • Reverse Transcriptase Polymerase Chain Reaction

Substances

  • MAS1 protein, human
  • Proto-Oncogene Mas
  • RNA, Small Interfering
  • Proto-Oncogene Proteins c-akt
  • Proto-Oncogene Proteins c-pim-1