The Origin of Stroma Influences the Biological Characteristics of Oral Squamous Cell Carcinoma

SIMPLE SUMMARY: Normal stromal cells play a significant role in the progression of cancers but are poorly investigated in oral squamous cell carcinoma (OSCC). In this study, we found that stromal cells derived from the gingival and periodontal ligament tissues could inhibit differentiation and promote the proliferation, invasion, and migration of OSCC both in vitro and in vivo. Furthermore, microarray data suggested that genes, such as CDK1, BUB1B, TOP2A, DLGAP5, BUB1, and CCNB2, probably play a role in influencing the different effects of gingival stromal tissue cells (G-SCs) and periodontal ligament stromal cells (P-SCs) on the progression of OSCC. Therefore, both G-SCs and P-SCs could promote the progression of OSCC, which could be a potential regulatory mechanism in the progression of OSCC. ABSTRACT: Normal stromal cells surrounding the tumor parenchyma, such as the extracellular matrix (ECM), normal fibroblasts, mesenchymal stromal cells, and osteoblasts, play a significant role in the progression of cancers. However, the role of gingival and periodontal ligament tissue-derived stromal cells in OSCC progression is unclear. In this study, the effect of G-SCs and P-SCs on the differentiation, proliferation, invasion, and migration of OSCC cells in vitro was examined by Giemsa staining, Immunofluorescence (IF), (3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium) (MTS), invasion, and migration assays. Furthermore, the effect of G-SCs and P-SCs on the differentiation, proliferation, and bone invasion by OSCC cells in vivo was examined by hematoxylin-eosin (HE) staining, immunohistochemistry (IHC), and tartrate-resistant acid phosphatase (TRAP) staining, respectively. Finally, microarray data and bioinformatics analyses identified potential genes that caused the different effects of G-SCs and P-SCs on OSCC progression. The results showed that both G-SCs and P-SCs inhibited the differentiation and promoted the proliferation, invasion, and migration of OSCC in vitro and in vivo. In addition, genes, including CDK1, BUB1B, TOP2A, DLGAP5, BUB1, and CCNB2, are probably involved in causing the different effects of G-SCs and P-SCs on OSCC progression. Therefore, as a potential regulatory mechanism, both G-SCs and P-SCs can promote OSCC progression.