AI Article Synopsis

  • * Researchers aimed to identify key genes in the TME that could be targeted for intervention in early stages of oral carcinogenesis, focusing on a specific gene, IL-1β, identified through systems biology and bioinformatics approaches.
  • * Experimental results showed that reducing IL-1β levels inhibited the growth of squamous cell carcinoma in lab tests, and targeting IL-1 in the TME using a receptor antagonist in a rat model successfully interrupted oral cancer development

Article Abstract

Head and neck squamous cell carcinoma (HNSCC) development is a multistage process includes the normal, dysplasia and squamous cell carcinoma (SCC) stages. Recently, increasing evidence has suggested that the tumor microenvironment (TME) is an integral part of malignant transformation. Exploring certain key node genes in TME for future intervention in dysplasia to interrupt oral carcinogenesis was the primary goal of this research. To achieve this goal, systems biology approaches were first applied to the epithelia and fibroblasts collected at sequential stages in a 4-nitroquinoline-1-oxide (4NQO) -induced rat oral carcinogenesis model. Through bioinformatics network construction, IL-1β was identified as one of the key node genes in TME during carcinogenesis. Immunohistochemical staining of human and rat samples demonstrated that IL-1β expression patterns were parallel to the stages of malignant transformation. Silencing IL-1β with lentivirus-delivered shRNA significantly inhibited oral squamous cell carcinoma cell growth both in vivo and in vitro. Based on these findings, we hypothesized that IL-1β may be a chemoprevention target in TME during oral carcinogenesis. Therefore, we targeted IL-1 in the TME by oral mucosal injection of an IL-1 receptor antagonist in 4NQO rats. The results demonstrated that targeting IL-1 could interrupt oral carcinogenesis by reprogramming the TME.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4735323PMC
http://dx.doi.org/10.1038/srep20208DOI Listing

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