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Article

The role of aplysia ras homolog I in colon cancer cell invasion and adhesion

  • Authors:
    • Jun Ouyang
    • Xiaohui Pan
    • Zecheng Hu
  • View Affiliations / Copyright

    Affiliations: Department of Gastrointestinal Surgery, The First Affiliated Hospital of University of South China, Hengyang, Hunan 421001, P.R. China, Department of Urology, The First Affiliated Hospital of University of South China, Hengyang, Hunan 421001, P.R. China
  • Pages: 5193-5199
    |
    Published online on: September 18, 2017
       https://doi.org/10.3892/etm.2017.5122
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Abstract

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.
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Copy and paste a formatted citation
Spandidos Publications style
Ouyang J, Pan X and Hu Z: The role of aplysia ras homolog I in colon cancer cell invasion and adhesion. Exp Ther Med 14: 5193-5199, 2017.
APA
Ouyang, J., Pan, X., & Hu, Z. (2017). The role of aplysia ras homolog I in colon cancer cell invasion and adhesion. Experimental and Therapeutic Medicine, 14, 5193-5199. https://doi.org/10.3892/etm.2017.5122
MLA
Ouyang, J., Pan, X., Hu, Z."The role of aplysia ras homolog I in colon cancer cell invasion and adhesion". Experimental and Therapeutic Medicine 14.5 (2017): 5193-5199.
Chicago
Ouyang, J., Pan, X., Hu, Z."The role of aplysia ras homolog I in colon cancer cell invasion and adhesion". Experimental and Therapeutic Medicine 14, no. 5 (2017): 5193-5199. https://doi.org/10.3892/etm.2017.5122
Copy and paste a formatted citation
x
Spandidos Publications style
Ouyang J, Pan X and Hu Z: The role of aplysia ras homolog I in colon cancer cell invasion and adhesion. Exp Ther Med 14: 5193-5199, 2017.
APA
Ouyang, J., Pan, X., & Hu, Z. (2017). The role of aplysia ras homolog I in colon cancer cell invasion and adhesion. Experimental and Therapeutic Medicine, 14, 5193-5199. https://doi.org/10.3892/etm.2017.5122
MLA
Ouyang, J., Pan, X., Hu, Z."The role of aplysia ras homolog I in colon cancer cell invasion and adhesion". Experimental and Therapeutic Medicine 14.5 (2017): 5193-5199.
Chicago
Ouyang, J., Pan, X., Hu, Z."The role of aplysia ras homolog I in colon cancer cell invasion and adhesion". Experimental and Therapeutic Medicine 14, no. 5 (2017): 5193-5199. https://doi.org/10.3892/etm.2017.5122
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