過去實驗室致力於探討Mitogen-Activated Protein Kinases/ Extracellular signal-Regulated Kinase (MAPK)訊息傳導路徑相關之微型核糖核酸 (miRNA)。在目前已知此訊息傳導路徑因突變而過度活化的黑色素細胞瘤 (melanoma) 中，發現諸多miRNA的過量表現 (overexpression) 均具有影響癌症相關細胞功能性能力，如增生(Proliferation)、遷移/侵襲 (Migration/Invasion)、凋亡 (Apoptosis)，認為此群miRNA具有癌症抑制基因(Tumor suppressor gene)之特質，並藉由抑制黑色素細胞瘤中可能產生預後不良的風險因子以及影響諸多與癌症進展相關之重要基因，希望將來成為有潛力的標靶治療手段。;We dedicated to investigating Mitogen-Activated Protein Kinases/ Extracellular signal-Regulated Kinase (MAPK) pathway-associated miRNAs in our previous study. While these miRNAs are overexpressed, it could suppress the multiple functional assays related to cancer development, such as proliferation, migration, invasion, and apoptosis in melanoma which harbored the mutation(s) to make MAPK pathway active. We hope that these miRNAs play the meaningful role as tumor suppressors and they could become the promising RNA interference drug against the specific cancer.
