Abstract 3069: The role of miR-30c-2* in clinical outcome and drug resistance in HPV-infected non-small cell lung cancer

Abstract

Abstract Lung cancer is leading cause of cancer death in Taiwanese women who are mostly to be life-time never smokers. Majority of drugs and combinations are used to treat with smoking lung cancer patients, not for nonsmokers. However, the 5-year survival rate in lung cancer patients remains ∼15% during the past three decades. Therefore, dissolving tumor recurrence and drug resistance is urgent needed for improving outcome in lung cancer, especially in nonsmokers. Mir-30c-2* has been considered to be tumor suppressor gene in various cancers. MiR-30c-2* levels were associated with in gemcitabine sensitivity of lung cancer cells. Down-regulation of miR-30c promotes tumor invasion via an increased in MTA1 expression. Our previous reports have indicated that HPV16/18 infection may be involved in Taiwanese lung tumorigenesis. Preliminary data showed that miR-30C-2* levels were elevated 45-fold in E6-knockdown TL-1 cells as compared with parental cells with non-specific RNAi tranfection. More interestingly, MTA-1 expression was negatively correlated with miR-30C-2* in lung tumors from lung cancer patients. Expression levels of MTA-1 were positive correlated with tumor stage and nodal metastasis in tumor tissues of lung cancer patients. Our cell model studies also found that miR-30C-2* suppressed by E6 could contribute to tumor metastasis and drug resistance via an increased in MTA-1 expression. These results were showed that miR-30C-2* levels in patients’ tumor tissues could be useful to predict outcome and therapeutic response and to select useful therapy drugs for lung cancer patients, especially in patients with HPV-infection. Citation Format: Ya-Wen Cheng, Hsiao-Ching Lin. The role of miR-30c-2* in clinical outcome and drug resistance in HPV-infected non-small cell lung cancer. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 3069. doi:10.1158/1538-7445.AM2015-3069