Abstract
Extracellular matrix (ECM) components are critical for all aspects of cell proliferation, adhesion, and morphological alteration. Recent progress has yielded multiple molecular drugs that specifically target gene products which are expressed at high levels in tumor cells. We investigated whether the sensitivity of tumor cells to molecular target drugs could be altered when cells were cultured on surfaces with various coating conditions such as lysine, laminin, Matrigel, collagen type I, and human fibronectin (HFN). This study evaluates the IC50 values of imatinib in oral squamous cell carcinoma (OSCC) cell lines when cells are cultured on plates coated with ECM components such as collagen type I and HFN. Four OSCC cell lines—SQUU-A, SQUU-B, SAS, and NA— are used. Cell proliferation was assessed using WST-8 reagent. Collagen type I and HFN significantly enhanced OSCC cell proliferation compared with control. Imatinib cytotoxicity was demonstrated following culture of OSCCs in culture plates coated with collagen type I or HFN. However, there were no significant changes in imatinib IC50 values between collagen type I and HFN. These results indicate that some molecular target drugs exhibit cancer cell cytotoxicity without being influenced by cell environment factors such as the ECM. These results may aid in the search for molecular target drugs to apply in the clinical chemotherapy of OSCC.
Highlights
Oral squamous cell carcinoma (OSCC) currently is treated largely by surgery and/or irradiation, few unequivocal controlled trials of treatment modalities have been conducted
We examined the effect of imatinib on OSCC cell proliferation and determined IC50 values for imatinib in OSCC cells cultured on plates coated with collagen type I or human fibronectin (HFN)
We found that collagen type I and HFN could effectively promote cell proliferation in OSCC cells, and there was no significant difference in IC50 values of imatinib
Summary
Oral squamous cell carcinoma (OSCC) currently is treated largely by surgery and/or irradiation, few unequivocal controlled trials of treatment modalities have been conducted. Anti-cancer drugs exhibit many mechanisms of action, including DNA synthesis antagonism and cell division disruption, but most require that the tumor cells are actively dividing. This targeting of actively-dividing cells by anti-cancer drugs leads to undesirable side effects. Molecular target drugs are developed following identification of gene products which are expressed at high levels in specific tumor cells. The establishment of fibrin-rich clots in wound spaces forms a provisional ECM, and clotting is accompanied by the activation of platelets, neutrophils, and macrophages These cells resolve wounds by promoting the synthesis, remodeling, and contraction of the matrix [11]. Integrin-mediated adhesion influences cell survival and may prevent programmed cell death [13]
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