Abstract
Abstract Aspirin is a 100 year old Non-steroidal anti-inflammatory drug (NSAID). Beside its use a cardio-protective agent, it is also used for treatment of headache, fever, and inflammation. Many studies have shown that regular intake of aspirin for 5 years or more reduces the risk of colon, breast, prostate, lung and skin cancers. However, mechanism for such actions is not very well understood. Since transformation of a normal cell to cancer cell often involves mutation and activation of proto-oncogene, we initiated this research to understand if aspirin modulates the level of oncogene products. In this study we focused on three different oncogenes; c-FOS, c-JUN and c-RAF. c-FOS and c-JUN are transcription factors, they form a heterodimer called Activator protein (AP-1) transcription factor and regulate the expression of other genes. We observed that, in serum starved HCT-116 colon cancer cells Aspirin and Salicylic acid inhibited serum induced c-FOS protein expression, however, levels of c-JUN protein were not inhibited. In fact Aspirin and Salicylic acid increased c-JUN levels marginally over the serum induced levels at all time points examined. Exposure of cells to Aspirin and Salicylic acid inhibited c-RAF levels in a concentration dependent fashion. Inhibition was observed at physiologically achieved concentration of 250 -500 micro molar Salicylic acid suggesting that Aspirin may mediate its effects through the formation of Salicylic acid. We are currently investigating how inhibition of c-RAF levels by Aspirin and Salicylic acid affects downstream signaling molecules such as p42/p44 MAP kinases. Modulation of proto oncogenes by Aspirin may represent an important pathway by which Aspirin may mediate its anti-cancer effects. Citation Format: Rakesh Dachineni, Goqiang Ai, Jayarama B. Gunaje. Aspirin modulates oncogene expression in hct 116 colon cancer cells. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 3501. doi:10.1158/1538-7445.AM2014-3501
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