Cyclophilin B promotes cell proliferation, migration, invasion and angiogenesis via regulating the STAT3 pathway in non-small cell lung cancer

Pathol Res Pract. 2019 Jun;215(6):152417. doi: 10.1016/j.prp.2019.04.009. Epub 2019 Apr 17.

Abstract

Lung cancer is the most common type of cancer and has become the leading cause of cancer-associated mortality worldwide. It has been reported that expression of Cyclophilin B was greatly elevated in the pancreatic cancer patient sera as compared with the healthy volunteer sera. This study aimed to investigate the role and regulatory mechanism of CypB in NSCLC progression. The expression levels of CypB was detected in NSCLC samples and cell lines by ELISA, western blot and immunohistochemistry assay. In addition, CCK8, colony formation, scratch and transwell assays were used to evaluate the proliferation, migration and invasion of A549 cells with CypB silencing. The expression of angiogenesis related proteins and pathway-related factors were detected by western blot. In NSCLC samples, CypB expression was upregulated. The expression of CypB was significantly reduced in the siRNA-cyclophilin B group. In addition, CypB silencing inhibited cell proliferation, migration and invasion. The expression of angiogenesis related proteins and pathway-related factors have also changed significantly. These findings suggested that CypB silencing may suppress the proliferation, invasion, migration and angiogenesis of A549 cells via inhibiting STAT3 pathway.

Keywords: Cyclophilin B; Invasion; Non-small cell lung cancer; Proliferation; STAT3.

MeSH terms

  • Aged
  • Aged, 80 and over
  • Carcinoma, Non-Small-Cell Lung / metabolism
  • Carcinoma, Non-Small-Cell Lung / pathology*
  • Cell Movement / physiology
  • Cell Proliferation / physiology
  • Cyclophilins / metabolism*
  • Female
  • Gene Expression Regulation, Neoplastic / physiology
  • Humans
  • Lung Neoplasms / metabolism
  • Lung Neoplasms / pathology*
  • Male
  • Neoplasm Invasiveness / pathology
  • Neovascularization, Pathologic / metabolism
  • Neovascularization, Pathologic / pathology*
  • STAT3 Transcription Factor / metabolism*
  • Signal Transduction / physiology

Substances

  • STAT3 Transcription Factor
  • STAT3 protein, human
  • cyclophilin B
  • Cyclophilins