Glucose and glutamine metabolism-related protein expression in breast ductal carcinoma in situ

Neoplasma. 2022 May;69(3):630-639. doi: 10.4149/neo_2022_220103N3. Epub 2022 Mar 10.

Abstract

Glucose and glutamine metabolism is involved in important tumor mechanisms. Metabolism-related protein expression has been previously reported to predict tumor prognosis. We aimed to investigate glucose and glutamine metabolism-related protein expression and its implication in breast ductal carcinoma in situ (DCIS). A tissue microarray was prepared for 205 DCIS cases. Glucose and glutamine metabolism-related proteins were immunostained. Based on the results of estrogen receptor, progesterone receptor, human epidermal growth factor receptor (HER)-2, and Ki-67, DCIS was classified into the luminal type, HER-2 type, and triple-negative breast cancer (TNBC). DCIS stroma was classified into non-inflammatory and inflammatory types per stromal histology. DCIS (N=205) was classified into luminal type (n=112), HER-2 type (n=81), and TNBC (n=12). Hexokinase II (p=0.044), GLS (p=0.003), and SLC7A5 (p<0.001) expression rates were the highest in TNBC. Inflammatory type stroma showed higher SLC7A5 (p<0.001) and SLC7A11 (p=0.008) expression rates than non-inflammatory type stroma. In summary, DCIS demonstrated differential expression of metabolism-related proteins according to the molecular subtype and stromal features. TNBC showed the highest glucose and glutamine metabolism-related protein expression, and inflammatory type stroma showed higher glutamine metabolism-related protein expression than non-inflammatory type stroma.

MeSH terms

  • Biomarkers, Tumor / metabolism
  • Breast Neoplasms*
  • Carcinoma, Ductal, Breast* / pathology
  • Carcinoma, Intraductal, Noninfiltrating*
  • Female
  • Glucose
  • Glutamine
  • Humans
  • Large Neutral Amino Acid-Transporter 1
  • Receptor, ErbB-2 / metabolism
  • Triple Negative Breast Neoplasms* / pathology

Substances

  • Biomarkers, Tumor
  • Large Neutral Amino Acid-Transporter 1
  • Glutamine
  • Receptor, ErbB-2
  • Glucose