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
AUTHORS (12)
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.
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