Objective: To investigate the role of biglycan (BGN) in colon cancer progression.
Methods: The association between BGN mRNA levels and the survival time of patients with colon cancer was analysed by referencing data from the Gene Expression Omnibus and The Cancer Genome Atlas (TCGA). Gene Set Enrichment Analysis (GSEA) was conducted to explore gene sets and pathways associated with BGN. In vitro analyses were undertaken in HCT116 cells to analyse cell proliferation, migration, invasion, cell cycle control and apoptosis. GSEA, Western blot analysis and small interfering RNAs were used to explore the molecular mechanisms of BGN in colon cancer cells.
Results: Analysis of the pairs of tissues from colon cancer patients showed that BGN protein levels were higher in colon cancer tissues compared with adjacent non-tumour tissues. High BGN levels were significantly associated with shorter survival times. BGN knockdown inhibited cell proliferation, migration and invasion; and induced cell cycle arrest in the G0/G1 phase and promoted apoptosis in HCT116 cells. GSEA found that BGN might affect tumour progression via the mitogen-activated protein kinase (MAPK) signalling pathway.
Conclusion: BGN might promote colon cancer progression via the MAPK signalling pathway and could be a potential target for future novel therapeutic strategies.
Keywords: Colon cancer; biglycan; invasion; mitogen-activated protein kinase; proliferation.