Afradi Zohreh, Panahipour Layla, Abbas Zadeh Salman, Gruber Reinhard
Department of Oral Biology, University Clinic of Dentistry, Medical University of Vienna, 1090 Vienna, Austria.
Epitome GmbH, 1100 Vienna, Austria.
Bioengineering (Basel). 2024 Jul 24;11(8):746. doi: 10.3390/bioengineering11080746.
Platelet-rich fibrin (PRF), originally used to support soft tissue healing, is also considered a therapeutic option for treating oral lichen planus and leukoplakia. The progression from the two premalignant lesions to the aggressive malignant oral squamous cell carcinoma involves an inflammatory process linked to chemokine expression. Thus, there is a rationale for studying how PRF modulates the expression of chemokines in oral squamous carcinoma cells. To this aim, we expose the oral squamous carcinoma cell line HSC2 to IL1β and TNFα either alone or in the presence of lysates obtained from solid PRF membranes. We report here that in HSC2 cells, PRF lysates significantly reduce the forced transcription of chemokines, e.g., CXCL1, CXCL2, CXCL8, CXCL10, and CCL5. Moreover, PRF lysates attenuate the nuclear translocation of p65 in HSC2 oral epithelial cells when exposed to IL1β and TNFα. PRF lysates further reduce chemokine expression provoked by poly:IC HMW. Even though less pronounced, PRF lysates reduce IL1β- and TNFα-induced chemokine expression in TR146 cells. In primary oral epithelial cells, however, PRF lysates increase the basal expression of CXCL1, CXCL2 and CXCL8. Thus, PRF can exert a biphasic effect on chemokine expression in oral squamous cell carcinoma cell lines and primary oral epithelial cells. These findings suggest that PRF may reduce inflammation in a malignant environment while provoking an immunological response in healthy oral epithelium.
富含血小板纤维蛋白(PRF)最初用于支持软组织愈合,现在也被视为治疗口腔扁平苔藓和白斑的一种治疗选择。从这两种癌前病变发展为侵袭性恶性口腔鳞状细胞癌涉及与趋化因子表达相关的炎症过程。因此,研究PRF如何调节口腔鳞状癌细胞中趋化因子的表达是有道理的。为了这个目的,我们将口腔鳞状癌细胞系HSC2单独或在存在从固态PRF膜获得的裂解物的情况下暴露于IL1β和TNFα。我们在此报告,在HSC2细胞中,PRF裂解物显著降低趋化因子(例如CXCL1、CXCL2、CXCL8、CXCL10和CCL5)的强制转录。此外,当暴露于IL1β和TNFα时,PRF裂解物减弱HSC2口腔上皮细胞中p65的核转位。PRF裂解物进一步降低由聚肌胞苷酸(poly:IC)高分子量(HMW)引发的趋化因子表达。尽管不太明显,但PRF裂解物降低TR146细胞中IL1β和TNFα诱导的趋化因子表达。然而,在原代口腔上皮细胞中,PRF裂解物增加CXCL1、CXCL2和CXCL8的基础表达。因此,PRF可对口腔鳞状癌细胞系和原代口腔上皮细胞中的趋化因子表达产生双相作用。这些发现表明,PRF可能在恶性环境中减轻炎症,同时在健康口腔上皮中引发免疫反应。