MiRNA-145 increases therapeutic sensibility to gemcitabine treatment of pancreatic adenocarcinoma cells
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Yong Lin1,2, Xin Ge3,4, Yiyang Wen3, Zhu-Mei Shi3,5, Qiu-Dan Chen2, Min Wang3, Ling-Zhi Liu6, Bing-Hua Jiang3,6, Yuan Lu1
1Department of Laboratory Medicine, Huashan Hospital of Fudan University, Shanghai, China
2The Department of Clinical Laboratory, Central Laboratory, Jing’an District Centre Hospital of Shanghai, Huashan Hospital of Fudan University Jing’An Branch, Shanghai, China
3State Key Lab of Reproductive Medicine, Key Laboratory of Human Functional Genomics of Jiangsu Province, Jiangsu Key Laboratory of Cancer Biomarkers, Prevention, and Treatment Department of Pathology, Cancer Center, Nanjing Medical University, Nanjing, China
4Ninggao Personalized Medicine and Technology Innovation Center, Nanjing, China
5Department of Neurosurgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China
6Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia, PA, United States of America
Yuan Lu, email: firstname.lastname@example.org
Keywords: pancreatic adenocarcinoma, gemcitabine, miR-145, p70S6K1, chemoresistance
Received: May 09, 2016 Accepted: August 25, 2016 Published: September 27, 2016
Pancreatic adenocarcinoma is one of the most leading causes of cancer-related deaths worldwide. Although recent advances provide various treatment options, pancreatic adenocarcinoma has poor prognosis due to its late diagnosis and ineffective therapeutic multimodality. Gemcitabine is the effective first-line drug in pancreatic adenocarcinoma treatment. However, gemcitabine chemoresistance of pancreatic adenocarcinoma cells has been a major obstacle for limiting its treatment effect. Our study found that p70S6K1 plays an important role in gemcitabine chemoresistance. MiR-145 is a tumor suppressor which directly targets p70S6K1 for inhibiting its expression in pancreatic adenocarcinoma, providing new therapeutic scheme. Our findings revealed a new mechanism underlying gemcitabine chemoresistance in pancreatic adenocarcinoma cells.
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