OSCC is the most common oral malignancy with a rapidly inclining mortality rate.Previous studies have reported that activated CXCR4 downregulates MMP-9 and MMP-13 via ERK pathway and thus promotes OSCC progression. Likewise, the silencing of CXCL12-CXCR4 will downregulate the expression of MMP-9 and MMP-13, which suppresses OSCC progression. Since previous studies rarely investigate silencing of CXCL12-CXCR4 in OSCC in terms of cell proliferation, and the molecular role of CXCR4 in OSCC cell proliferation has not been determined yet, this study investigates theeffect of blocking CXCL12-CXCR4 signaling pathway on OSCC treatment, both invivo and in vitro. The study will use U698 and K562 cell lines,which express high and low CXCR4, with negative control (saline), positive control (Taxol), or an increasing amount of AMD3100, a CXCR4 antagonist.Employing a variety of methods, both in vitro, such as MTT, colony formation assay, and western blot, and in vivo, such as U698 or K562 mice xenografts, the paper investigates whether or not AMD3100 would effectively reduce CXCR4 and provide enhanced inhibition on OSCC cell proliferation.
Keywords: OSCC,CXCL12-CXCR4 Pathway, AMD3100, Proliferation
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