Micro-RNA-155 is induced by K-Ras oncogenic signal and promotes ROS stress in pancreatic cancer

0301 basic medicine Forkhead Box Protein O3 Lentivirus Mice, Nude Forkhead Transcription Factors Antioxidants 3. Good health Gene Expression Regulation, Neoplastic Pancreatic Neoplasms Mice MicroRNAs 03 medical and health sciences Cell Transformation, Neoplastic Genes, ras Cell Line, Tumor Doxycycline Animals Humans Female Reactive Oxygen Species Oxidation-Reduction Neoplasm Transplantation Signal Transduction
DOI: 10.18632/oncotarget.4125 Publication Date: 2015-09-15T04:49:54Z
ABSTRACT
// Peng Wang 1,2,* , Chao-feng Zhu 1,* Ming-zhe Ma Gang Chen 3,* Ming Song 1 Zhao-lei Zeng Wen-hua Lu Jing Yang Shijun Wen Paul J. Chiao 4 Yumin Hu and Huang 1,3 Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center Medicine, Guangzhou, China 2 Department Emergency Memorial Hospital, 3 Translational Molecular Pathology, The Texas MD Anderson Houston, TX, USA Cellular Oncology, * These authors contributed equally to this work Correspondence to: Hu, email: Huang, Keywords : K-Ras, miR-155, reactive oxygen species, pancreatic cancer Received November 05, 2014 Accepted May 02, 2015 Published 12, Abstract oncogenic K-Ras can transform various mammalian cells plays a critical role development cancer. MicroRNAs (miRNA) have been shown contribute tumorigenic progression. However, the nature miRNAs involved transformation remains be investigated. Here, by using microarray we identified miR-155 as most upregulated miRNA after both acute prolonged activation doxycyline-inducible system. Pharmacological inhibition MAPK NF-κB pathway blocked induction response activation. Overexpression caused Foxo3a, leading decrease major antioxidants including SOD2 catalase, enhanced cell proliferation induced ROS generation. Importantly, correlations Foxo3a were also validated human tissues. Therefore, propose that an important mediated cellular redox regulation.
SUPPLEMENTAL MATERIAL
Coming soon ....
REFERENCES (34)
CITATIONS (96)