Oral cancer is one of the serious life-threatening diseases in the world. In addition to surgery, the conventional treatment for oral cancer includes radiation and anti-cancer drugs, which usually act by induction of DNA damage. However, approximately one-third of treated patients will experience local or regional recurrence. G9a is a histone methyltransferase responsible for mono- or dimethylation of lysine 9 in histone H3. Our recent work has demonstrated that G9a level is highly correlated with aggressiveness and poor prognosis of lung, ovarian and colon cancer patients in Taiwanese population. Here, we report that knockdown of G9a resulted in decrease cell survival and cologenic capacity following DNA damage induced independently by etoposide and ionizing radiation. Depletion of G9a caused sustained phosphorylation of γ-H2AX after etoposide treatment. Together, our data suggest that a novel function of G9a may increase the DNA repair efficiency and promote the oral cancer cells recovery and survival from the DNA damage agents. We suggest that G9a may contribute to oral cancer proliferation by improvement of homologous recombination repair of DNA double break. Our study paves the way for exploring the blockade of G9a overexpression as a novel approach for the prevention and treatment of oral cancer.
Citation Format: Chia-Wen Liu, Shih-Ting Cha, Ching-Ting Tan, Min-Liang Kuo. Histone methyltransferase G9a promotes the oral cancer cells recovery from drug-induced DNA damage. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 4063. doi:10.1158/1538-7445.AM2013-4063