CALCR knockdown inhibits the development and progression of non-small-cell lung cancer

Carcinogenesis. 2021 Nov 12;42(11):1390-1398. doi: 10.1093/carcin/bgab076.

Abstract

G-protein-coupled receptors (GPCRs) have been reported to participate in the occurrence and development of a variety of human cancers. CALCR is one of the hundreds of GPCRs, but its expression level and functional importance have never been investigated in non-small-cell lung cancer (NSCLC). In the present study, the protein expression level of CALCR was detected by immunohistochemical staining and western blot analysis. The Celigo cell counting assay was used to assess cell proliferation. Both the wound-healing assay and the transwell assay were performed to evaluate cell migration. Flow cytometric analysis was utilized to detect cell apoptosis and cell cycle. A mouse xenograft model was constructed to conduct the in vivo experiments. The results indicated that the CALCR expression was abundantly up-regulated in NSCLC and positively related to tumor infiltrate. Besides, CALCR knockdown could significantly suppress cell proliferation, migration, enhance apoptosis and arrest cell cycle. The in vivo study verified the inhibitory effects of CALCR knockdown on NSCLC tumorigenesis. The abovementioned results provided a reference for the treatment of NSCLC, that was, CALCR knockdown might be a considerable therapeutic strategy.

MeSH terms

  • Animals
  • Calcitonin Receptor-Like Protein / genetics*
  • Carcinoma, Non-Small-Cell Lung / genetics
  • Carcinoma, Non-Small-Cell Lung / pathology*
  • Disease Progression
  • Female
  • Flow Cytometry
  • Gene Knockdown Techniques*
  • Heterografts
  • Humans
  • Lung Neoplasms / genetics
  • Lung Neoplasms / pathology*
  • Male
  • Mice
  • Middle Aged

Substances

  • CALCRL protein, human
  • Calcitonin Receptor-Like Protein