Alcohol promotes epithelial mesenchymal transformation-mediated premetastatic niche formation of colorectal cancer by activating interaction between laminin-γ2 and integrin-β1

World J Gastroenterol. 2022 Sep 21;28(35):5154-5174. doi: 10.3748/wjg.v28.i35.5154.

Abstract

Background: Colorectal cancer (CRC) is a common malignant tumor. Alcohol consumption is positively correlated with CRC malignant metastasis; however, the mechanism is unclear. The interaction between laminin-γ2 (LAMC2) and integrin-β1 (ITGB1) plays a role in premetastatic niche signaling, which may induce epithelial mesenchymal transformation (EMT) and lead to metastasis.

Aim: To investigate the effects of alcohol on CRC metastasis from the molecular mechanism of the premetastatic niche.

Methods: The interaction between LAMC2 and ITGB1 was measured by Duolink assay, and the expression levels of LAMC2, ITGB1 and focal adhesion kinase (FAK), snail, fibronectin, N-cadherin and special AT-rich sequence binding protein 1 (SATB1) were measured by quantitative real-time polymerase chain reaction, immunohistochemistry and western blotting. Interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) and IL-6 levels were measured via enzyme-linked immunosorbent assay, histopathological assessment via hematoxylin eosin staining, and determination of aberrant crypt foci via methylene blue.

Results: The lymph node metastasis rate was higher in the alcohol group than non-alcohol group. There was a significant increase in interaction signals between LAMC2 and ITGB1, and an increase in phosphorylate-FAK/FAK, snail, fibronectin, N-cadherin and SATB1, whereas E-cadherin was reduced in the alcohol group compared to the non-alcohol group in both animal and clinical samples. Serum IL-1β, TNF-α and IL-6 were higher in alcohol group than in non-alcohol group. Alcohol may promote CRC metastasis by influencing the molecular mechanism of the premetastatic niche.

Conclusion: Our study suggests that alcohol promotes EMT-mediated premetastatic niche formation of CRC by activating the early interaction between LAMC2 and ITGB1 and lead to CRC metastasis.

Keywords: Alcohol; Colorectal cancer; Epithelial mesenchymal transformation; Metastasis; Premetastatic niche.

MeSH terms

  • Animals
  • Cadherins
  • Cell Line, Tumor
  • Cell Movement
  • Colorectal Neoplasms* / pathology
  • Eosine Yellowish-(YS) / pharmacology
  • Epithelial-Mesenchymal Transition
  • Fibronectins / pharmacology
  • Focal Adhesion Protein-Tyrosine Kinases / metabolism
  • Hematoxylin / pharmacology
  • Integrin beta1 / metabolism
  • Integrin beta1 / pharmacology
  • Interleukin-1beta
  • Interleukin-6
  • Laminin
  • Matrix Attachment Region Binding Proteins*
  • Methylene Blue
  • Tumor Necrosis Factor-alpha / pharmacology

Substances

  • Cadherins
  • Fibronectins
  • Integrin beta1
  • Interleukin-1beta
  • Interleukin-6
  • Laminin
  • Matrix Attachment Region Binding Proteins
  • Tumor Necrosis Factor-alpha
  • Focal Adhesion Protein-Tyrosine Kinases
  • Methylene Blue
  • Eosine Yellowish-(YS)
  • Hematoxylin