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Lentiviral vector-mediated IL-9 overexpression stimulates cell proliferation by targeting c-myc and cyclin D1 in colitis-associated cancer
Colorectal cancer caused by inflammatory bowel disease is referred as colitis-associated cancer (CAC). The mechanism underling CAC is not fully understood. In the present study, the role of interleukin-9 (IL-9) in CAC was examined. The current study included 12 colorectal tissue specimens and matche...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6313219/ https://www.ncbi.nlm.nih.gov/pubmed/30655753 http://dx.doi.org/10.3892/ol.2018.9567 |
Sumario: | Colorectal cancer caused by inflammatory bowel disease is referred as colitis-associated cancer (CAC). The mechanism underling CAC is not fully understood. In the present study, the role of interleukin-9 (IL-9) in CAC was examined. The current study included 12 colorectal tissue specimens and matched adjacent tissues from CAC. The expression of IL-9 protein was examined using immunohistochemical staining. The expression of IL-9 in cancer tissues was markedly higher compared with that in adjacent tissues. Furthermore, IL-9 gene overexpression lentiviral vectors were constructed to overexpress IL-9 in RKO and Caco-2 cell lines. The role of IL-9 in cell proliferation was investigated using a Cell Counting Kit-8 assay, and MYC proto-oncogene bHLH transcription factor (c-Myc) and cyclinD1 expression levels were detected by reverse transcription-quantitative polymerase chain reaction. Notably, IL-9 overexpression promoted the proliferation of colonic epithelial cells by upregulating of the expression of c-Myc and cyclinD1. In conclusion, the present results suggested that IL-9 may exhibit an essential role in the pathogenesis of CAC, and IL-9 promotes the proliferation of colonic epithelial RKO and Caco2 cells, partially via the upregulation of c-Myc and cyclinD1 expression. |
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