Nature Communications (Feb 2017)
Mutant Kras- and p16-regulated NOX4 activation overcomes metabolic checkpoints in development of pancreatic ductal adenocarcinoma
- Huai-Qiang Ju,
- Haoqiang Ying,
- Tian Tian,
- Jianhua Ling,
- Jie Fu,
- Yu Lu,
- Min Wu,
- Lifeng Yang,
- Abhinav Achreja,
- Gang Chen,
- Zhuonan Zhuang,
- Huamin Wang,
- Deepak Nagrath,
- Jun Yao,
- Mien-Chie Hung,
- Ronald A. DePinho,
- Peng Huang,
- Rui-Hua Xu,
- Paul J. Chiao
Affiliations
- Huai-Qiang Ju
- Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine
- Haoqiang Ying
- Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center
- Tian Tian
- Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine
- Jianhua Ling
- Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center
- Jie Fu
- Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center
- Yu Lu
- Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center
- Min Wu
- Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center
- Lifeng Yang
- Laboratory for Systems Biology of Human Diseases, Rice University
- Abhinav Achreja
- Laboratory for Systems Biology of Human Diseases, Rice University
- Gang Chen
- Department of Translational Molecular Pathology, The University of Texas MD Anderson Cancer Center
- Zhuonan Zhuang
- Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center
- Huamin Wang
- Department of Pathology, The University of Texas MD Anderson Cancer Center
- Deepak Nagrath
- Laboratory for Systems Biology of Human Diseases, Rice University
- Jun Yao
- Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center
- Mien-Chie Hung
- Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center
- Ronald A. DePinho
- The University of Texas Graduate School of Biomedical Sciences
- Peng Huang
- Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine
- Rui-Hua Xu
- Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine
- Paul J. Chiao
- Department of Molecular and Cellular Oncology, The University of Texas MD Anderson Cancer Center
- DOI
- https://doi.org/10.1038/ncomms14437
- Journal volume & issue
-
Vol. 8,
no. 1
pp. 1 – 14
Abstract
Kras activation and p16 inactivation cooperatively promote pancreatic cancer progression. Here, the authors show that such cooperation depends upon an increased expression of the NAD(P)H oxidase NOX4 achieved through transcription factors independently regulated by the two oncogenic genetic alterations.
