PRF Lysates Modulate Chemokine Expression in Oral Squamous Carcinoma and Healthy Epithelial Cells

Author:

Afradi Zohreh1,Panahipour Layla1ORCID,Abbas Zadeh Salman2ORCID,Gruber Reinhard134

Affiliation:

1. Department of Oral Biology, University Clinic of Dentistry, Medical University of Vienna, 1090 Vienna, Austria

2. Epitome GmbH, 1100 Vienna, Austria

3. Department of Periodontology, School of Dental Medicine, University of Bern, 3010 Bern, Switzerland

4. Austrian Cluster for Tissue Regeneration, 1200 Vienna, Austria

Abstract

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.

Funder

University Clinic of Dentistry

Publisher

MDPI AG

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