Differential expression of Kindlin-1 and Kindlin-2 correlates with esophageal cancer progression and epidemiology

Sci China Life Sci. 2017 Nov;60(11):1214-1222. doi: 10.1007/s11427-016-9044-5. Epub 2017 Jun 29.

Abstract

Esophageal cancer (EC) is one of the most lethal malignancies in China, but the etiology and risk factors remain unclear. The integrin-interacting proteins Kindlin-1 and Kindlin-2 are focal adhesion molecules that activate transmembrane receptor integrins and regulate tumor cell growth, invasion, and metastasis. Here, we report that Kindlin-1 and Kindlin-2 are differentially expressed among Chinese EC patients. For this, Kindlin-1 and Kindlin-2 expression was evaluated in 220 EC patients by immunohistochemistry (IHC) and found to be correlated with the EC progression, along with a variety of epidemiologic parameters, including smoking, family EC history, and EC invasion status. Moreover, data downloaded from the Oncomine database revealed that both Kindlin-1 and Kindlin-2 were upregulated in ECs compared with normal esophageal tissues; although Kindlin-1 was highly expressed in well-differentiated tumors, whereas Kindlin-2 was more prevalent in poorly differentiated tumors. Collectively, these data suggest that Kindlin-1 may inhibit, while Kindlin-2 may promote, EC progression. This study, for the first time, linked the expression of Kindlin-1 and Kindlin-2 with EC family genetic background and living habits, which may help further our understanding of the various causes of EC.

Keywords: Kindlin-1; Kindlin-2; epidemiology; esophageal cancer.

MeSH terms

  • Biomarkers, Tumor
  • Cells, Cultured
  • China / epidemiology
  • Disease Progression
  • Esophageal Neoplasms / epidemiology
  • Esophageal Neoplasms / genetics*
  • Esophageal Neoplasms / physiopathology*
  • Female
  • Gene Expression Regulation, Neoplastic*
  • Genetic Association Studies
  • Humans
  • Immunohistochemistry
  • Male
  • Membrane Proteins / genetics*
  • Membrane Proteins / metabolism*
  • Middle Aged
  • Neoplasm Invasiveness
  • Neoplasm Proteins / genetics*
  • Neoplasm Proteins / metabolism*
  • Risk Factors

Substances

  • Biomarkers, Tumor
  • FERMT1 protein, human
  • FERMT3 protein, human
  • Membrane Proteins
  • Neoplasm Proteins