PKB/Akt-dependent regulation of inflammation in cancer

Semin Cancer Biol. 2018 Feb:48:62-69. doi: 10.1016/j.semcancer.2017.04.018. Epub 2017 May 2.

Abstract

Chronic inflammation is a major cause of human cancer. Clinical cancer therapies against inflammatory risk factors are strategically determined. To rationally guide a novel drug development, an improved mechanistic understanding on the pathological connection between inflammation and carcinogenesis is essential. PI3K-PKB signaling axis has been extensively studied and shown to be one of the key oncogenic drivers in most types of cancer. Pharmacological inhibition of the components along this signaling axis is of great interest for developing novel therapies. Interestingly, emerging studies have shown a close association between PKB activation and inflammatory activity in the vicinity of the tumor, and either blockade of PKB or attenuation of para-tumoral inflammation reveals a mutual-interactive pattern through pathway crosstalk. In this review, we intend to discuss recent advances of PKB-regulated chronic inflammation and its potential impacts on tumor development.

Keywords: Chronic inflammation; Immune surveillance; Immunogenic cancer progression; Intratumoral immune response; Oncogenic signaling; Protein kinase B.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Cell Differentiation / immunology
  • Cell Movement / immunology
  • Enzyme Activation
  • Humans
  • Inflammation / drug therapy
  • Inflammation / metabolism*
  • Macrophages / enzymology
  • Molecular Targeted Therapy
  • Neoplasms / immunology*
  • Neoplasms / metabolism
  • Neoplasms / physiopathology*
  • Proto-Oncogene Proteins c-akt / metabolism*
  • Signal Transduction

Substances

  • Proto-Oncogene Proteins c-akt