We are using cookies to implement functions like login, shopping cart or language selection for this website. Furthermore we use Google Analytics to create anonymized statistical reports of the usage which creates Cookies too. You will find more information in our privacy policy.
OK, I agree I do not want Google Analytics-Cookies
International Poster Journal of Dentistry and Oral Medicine



Forgotten password?


Int Poster J Dent Oral Med 16 (2014), DGMKG     11. June 2014
Int Poster J Dent Oral Med 16 (2014), DGMKG  (11.06.2014)

Supplement, Poster 775, Language: German/English

The influence of Paraoxonase-2 (PON-2) on resistance against radiotherapy in oral squamous cell carcinoma
Krüger, Maximilian / Moergel, Maximilian / Horke, Sven / Al-Nawas, Bilal
Background: In oral cancer apoptosis induction is a key mechanism of radiotherapy. Upregulation of antiapoptotic proteins inside the tumor leads to an advantage for survival under therapy. In vascular cells Paraoxonase-2 (PON-2) reduces overwhelming ROS-production with the potential to prevent endothelial cells to undergo mitochondrial induced apoptosis. Since irradiation typically induces elevated levels of ROS, PON-2 could also protect squamous cell carcinoma against oxidative stress. Further, some cancers (liver, oesophagus, lymphatic tissue) showed overexpression of PON-2. For today expression pattern and functional influence of PON-2 in squamous cell carcinoma of the head and neck has not been investigated.
Methods: Basal PON-2 expression was determined in vitro in four squamous cell carcinoma cell lines and in human specimen of five patients with oral cancer by western blot analysis. Induction of PON-2 protein expression after singular radiation with 7 Gray 24, 48 and 72 hours after irradiation was examined also. Simultaneously, activity of Caspase 3/7 was examined for apoptosis detection after singular irradiation and temporary PON-2 knockdown by siRNA treatment.
Results: A variable PON-2 expression pattern in vitro and in vivo was detected. Intriguingly, higher basal levels of PON-2 seem to protect cells against radiation-induced apoptosis., while singular irradiation leads to induction of PON-2. On the other hand, temporary PON-2 knockdown leads to elevated apoptosis after irradiation.
Discussion: While some tumors showed higher levels of basal PON-2 expression, other tumors upregulated PON-2 as response to therapy. Tumor cells with higher expression levels of PON-2 basal or as response to therapy may have a biological advantage to suppress irradiation induced apoptosis.

Keywords: Oral cancer, ROS, PON-2, irradiation therapy

64. Kongress der Deutschen Gesellschaft für Mund-, Kiefer- und Gesichtschirurgie (DGMKG)
11.-14. Juni 2014
Mainz, Deutschland