Low glucose dependent decrease of apoptosis and induction of autophagy in breast cancer MCF-7 cells

Mol Cell Biochem. 2016 Jun;417(1-2):35-47. doi: 10.1007/s11010-016-2711-4. Epub 2016 May 9.

Abstract

Cancer cells have developed a number of adaptation mechanisms involving the signal activation of the transduction pathways, which promotes the progression and metastasis. Our results showed that the percentage of apoptotic MCF-7 cells incubated in the low glucose medium for 48 h was lower in comparison to those cultured in the high glucose medium, despite the high expression of the proapoptotic transcription factor-CHOP. Furthermore, the MCF-7 cells incubated in the low glucose medium for 48 h showed a higher expression of NF-κB p100/p52 subunits compared to cells incubated in the high glucose medium. Moreover, our findings demonstrated that the shortage of glucose strongly induces autophagy in MCF-7 cells. The activation of this process is not associated with the changes in the expression of mTOR kinase. We suggest, that the antiapoptotic chaperone ORP150 induction, transcription factor NF-κB2 activation, and increased autophagy constitute mechanisms protecting the MCF-7 cells against apoptosis.

Keywords: Apoptosis; Autophagy; CHOP; NF-κB2; ORP150; mTOR.

MeSH terms

  • Apoptosis*
  • Autophagy*
  • Breast Neoplasms / genetics
  • Breast Neoplasms / metabolism*
  • Breast Neoplasms / pathology
  • Female
  • Glucose / genetics
  • Glucose / metabolism*
  • HSP70 Heat-Shock Proteins / genetics
  • HSP70 Heat-Shock Proteins / metabolism
  • Humans
  • MCF-7 Cells
  • NF-kappa B p52 Subunit / genetics
  • NF-kappa B p52 Subunit / metabolism
  • Neoplasm Proteins / genetics
  • Neoplasm Proteins / metabolism
  • TOR Serine-Threonine Kinases / genetics
  • TOR Serine-Threonine Kinases / metabolism
  • Transcription Factor CHOP / genetics
  • Transcription Factor CHOP / metabolism

Substances

  • DDIT3 protein, human
  • HSP70 Heat-Shock Proteins
  • NF-kappa B p52 Subunit
  • Neoplasm Proteins
  • oxygen-regulated proteins
  • Transcription Factor CHOP
  • MTOR protein, human
  • TOR Serine-Threonine Kinases
  • Glucose