Pro-inflammatory Genes as Biomarkers and Therapeutic Targets in Oral Squamous Cell Carcinoma

Coassembled nanostructured bioscaffold reduces the expression of proinflammatory cytokines to induce apoptosis in epithelial cancer cells

“…Previous studies of the SCC25 cell line in comparison with normal human oral keratinocytes revealed significant over expression of the pro-inflammatory cytokine response, upregulation of the cytokinesis promoting genes 42 and, in particular, increased expression of NF useful here as an easily characterised component of a larger inflammatory pathway 43 . The uncontrolled G2 to M cell cycle progression is essential for oral cancer progression, and is characterised by an increase in the tumour size 43 . The transcription factors associated with this pathway, PLK1 and FOXM1, activate CEP55, a cytokinesis promoter identified as a key marker of tumor formation and progression 44 .…”

The importance of oncogenic transcription factors for oral cancer pathogenesis and treatment

“…This approach entraps activated TFs in the cytoplasm, thus preventing them from binding to their target gene promoter. This technology has been applied efficiently in cell culture [50][51][52][53][54] Growth inhibition 23 neoplasm 55 5 b-catenin Nuclear overexpression, 25 oral cancer progression, 26 metastasis [56][57][58] Inhibits transcription and invasion 59 6 Snail Overexpression, 60 activation, 61 invasion, 61 correlated with EMT [27][28][29] Reduces cancer stemness property 62 7 HIF1a…”

Cellular changes in the tumor microenvironment of human esophageal squamous cell carcinomas

“…Furthermore, we have also found that some of the DCs in ESCC stroma can express the tryptophan-catabolizing enzyme IDO [23], which has been shown to be a critical factor in inducing T cell tolerance and promoting cancer progression in various human cancers. Such alternation in microenvironmental is a common event in many types of SCCs, and the investigation of microenvironmental changes in ESCCs may have a widely clinical significance [5,6,17,24]. Therefore, efforts to understand the role of tumor stroma response in the progression of human SCCs have been made [7,8,25] because a better understanding of the cellular response of tumor stroma in regulating cancer progression will lead to novel therapeutic interventions.…”

“…Bergman and colleagues have revealed that COX-2 can stimulate the expansion of T regulatory type I cells and then inhibit host immunity in head and neck SCCs [14]. Furthermore, Moussai et al reported that increased lymphatic microvessel density and macrophage derived VEGF-C in human cutaneous SCCs [15]; others have examined the significance of fibroblasts [16] and the possibility of proinflammatory genes as biomarkers and therapeutic targets in oral SCC [17]. Many types of inflammatory cells have been implicated in the characterization of human SCC or ESCC tumor microenvironment [3,15,16,18,19].…”