Aplysia ras homolog I (ARHI) acts as a tumor suppressor in certain cancer cells. However, the role of ARHI in colon cancer development has not previously been reported. The present study aimed to investigate the functional role of ARHI in colon cancer focusing on the aspect of metastasis. Furthermore, the molecular mechanism underlying its function was explored. The present study detected the expression of ARHI in a human colon epithelial cell line and colon cancer cell lines using reverse transcription‑quantitative polymerase chain reaction and western blotting analysis. It was demonstrated that ARHI expression was significantly downregulated in colon cancer cell lines compared with the normal colon epitheli... More
Aplysia ras homolog I (ARHI) acts as a tumor suppressor in certain cancer cells. However, the role of ARHI in colon cancer development has not previously been reported. The present study aimed to investigate the functional role of ARHI in colon cancer focusing on the aspect of metastasis. Furthermore, the molecular mechanism underlying its function was explored. The present study detected the expression of ARHI in a human colon epithelial cell line and colon cancer cell lines using reverse transcription‑quantitative polymerase chain reaction and western blotting analysis. It was demonstrated that ARHI expression was significantly downregulated in colon cancer cell lines compared with the normal colon epithelial cell line (P<0.05). An ARHI‑pcDNA3.1 plasmid was transfected into HCT116 cells to overexpress ARHI. The number of invaded cells and the adhesive ability were significantly decreased in the ARHI overexpression group compared with the control group, as determined by cell invasion and adhesion assays (P<0.05). Furthermore, ARHI overexpression led to increased mRNA and protein expression levels of E‑cadherin, and decreased mRNA and protein expression levels of N‑cadherin and vimentin. Wnt/β‑catenin signaling was suppressed in HCT116 cells overexpressing ARHI. Lithium chloride, a wnt/β‑catenin signaling activator, was able to attenuate the effect of ARHI on HCT116 cell invasion and adhesion. In addition, the effect of ARHI on epithelial‑mesenchymal transition (EMT) in HCT116 cells was reversed by the activation of wnt/β‑catenin signaling. In conclusion, the present study provided novel evidence that ARHI could inhibit colon cancer cell invasion and adhesion through suppressing EMT, and these effects were achieved, at least partially, via the suppression of the wnt/β‑catenin signaling pathway. The present findings may help in developing novel therapeutic approaches for colon cancer.
