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3. WITHDRAWN: NNK promotes chronic pancreatitis to pancreatic intraepithelial neoplasia and accelerates pancreatic cancer migration

Author

Chen, Xin, primary, Sheng, Liang, additional, Ma, Jiguang, additional, Jiang, Zhengdong, additional, Xu, Qinhong, additional, Lei, Jianjun, additional, Duan, Wanxing, additional, Nan, Ligang, additional, Li, Xuqi, additional, Wang, Zheng, additional, Wu, Zheng, additional, Xu, Jun, additional, Wang, Fengfei, additional, Huang, Jason H., additional, Wu, Erxi, additional, Ma, Qingyong, additional, and Zhang, Dong, additional

Published
2017
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4. Reactive Oxygen Species and Targeted Therapy for Pancreatic Cancer

Author

Zhang, Lun, Li, Jiahui, Zong, Liang, Chen, Xin, Chen, Ke, Jiang, Zhengdong, Nan, Ligang, Li, Xuqi, Li, Wei, Shan, Tao, Ma, Qingyong, and Ma, Zhenhua

Subjects
Article Subject
Abstract

Pancreatic cancer is the fourth leading cause of cancer-related death in the United States. Reactive oxygen species (ROS) are generally increased in pancreatic cancer cells compared with normal cells. ROS plays a vital role in various cellular biological activities including proliferation, growth, apoptosis, and invasion. Besides, ROS participates in tumor microenvironment orchestration. The role of ROS is a doubled-edged sword in pancreatic cancer. The dual roles of ROS depend on the concentration. ROS facilitates carcinogenesis and cancer progression with mild-to-moderate elevated levels, while excessive ROS damages cancer cells dramatically and leads to cell death. Based on the recent knowledge, either promoting ROS generation to increase the concentration of ROS with extremely high levels or enhancing ROS scavenging ability to decrease ROS levels may benefit the treatment of pancreatic cancer. However, when faced with oxidative stress, the antioxidant programs of cancer cells have been activated to help cancer cells to survive in the adverse condition. Furthermore, ROS signaling and antioxidant programs play the vital roles in the progression of pancreatic cancer and in the response to cancer treatment. Eventually, it may be the novel target for various strategies and drugs to modulate ROS levels in pancreatic cancer therapy.

Published
2016
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6. β2-Adrenogenic signaling regulates NNK-induced pancreatic cancer progression via upregulation of HIF-1α

Author

Zhang, Dong, primary, Lei, Jianjun, additional, Ma, Jiguang, additional, Chen, Xin, additional, Sheng, Liang, additional, Jiang, Zhengdong, additional, Nan, Ligang, additional, Xu, Qinhong, additional, Duan, Wanxing, additional, Wang, Zheng, additional, Li, Xuqi, additional, Wu, Zheng, additional, Wu, Erxi, additional, Ma, Qingyong, additional, and Huo, Xiongwei, additional

Published
2015
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7. miR-221/222 induces pancreatic cancer progression through the regulation of matrix metalloproteinases

Author

Xu, Qinhong, primary, Li, Pei, additional, Chen, Xin, additional, Zong, Liang, additional, Jiang, Zhengdong, additional, Nan, Ligang, additional, Lei, Jianjun, additional, Duan, Wanxing, additional, Zhang, Dong, additional, Li, Xuqi, additional, Sha, Huanchen, additional, Wu, Zheng, additional, Ma, Qingyong, additional, and Wang, Zheng, additional

Published
2015
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8. Ginkgolic acid suppresses the development of pancreatic cancer by inhibiting pathways driving lipogenesis

Author

Ma, Jiguang, primary, Duan, Wanxing, additional, Han, Suxia, additional, Lei, Jianjun, additional, Xu, Qinhong, additional, Chen, Xin, additional, Jiang, Zhengdong, additional, Nan, Ligang, additional, Li, Jiahui, additional, Chen, Ke, additional, Han, Liang, additional, Wang, Zheng, additional, Li, Xuqi, additional, Wu, Erxi, additional, and Huo, Xiongwei, additional

Published
2015
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9. Overexpression of Nodal induces a metastatic phenotype in pancreatic cancer cells via the Smad2/3 pathway

Author

Duan, Wanxing, primary, Li, Rong, additional, Ma, Jiguang, additional, Lei, Jianjun, additional, Xu, Qinhong, additional, Jiang, Zhengdong, additional, Nan, Ligang, additional, Li, Xuqi, additional, Wang, Zheng, additional, Huo, Xiongwei, additional, Han, Liang, additional, Wu, Zheng, additional, Wu, Erxi, additional, and Ma, Qingyong, additional

Published
2015
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10. β2-adrenogenic signaling regulates NNK-induced pancreatic cancer progression via upregulation of HIF-1α.

Author

Zhang D, Lei J, Ma J, Chen X, Sheng L, Jiang Z, Nan L, Xu Q, Duan W, Wang Z, Li X, Wu Z, Wu E, Ma Q, and Huo X

Subjects
Aged, Animals, Cell Line, Tumor, Cell Proliferation drug effects, Disease Progression, Female, Gene Knockdown Techniques, Humans, Hypoxia-Inducible Factor 1, alpha Subunit biosynthesis, Hypoxia-Inducible Factor 1, alpha Subunit genetics, Mice, Mice, Nude, Middle Aged, Pancreatic Neoplasms chemically induced, Pancreatic Neoplasms metabolism, Receptors, Adrenergic, beta-2 biosynthesis, Signal Transduction, Smoking metabolism, Transcriptional Activation, Up-Regulation, Carcinogens pharmacology, Hypoxia-Inducible Factor 1, alpha Subunit metabolism, Nitrosamines pharmacology, Pancreatic Neoplasms etiology, Pancreatic Neoplasms pathology, Receptors, Adrenergic, beta-2 metabolism
Abstract

Cigarette smoking is a risk factor for pancreatic cancer. It is suggested that 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), a tobacco-specific nitrosamine, mediates the carcinogenic action of cigarette smoking by promoting cancer growth. In the present study, we show that smoking, HIF-1α expression and β2-adrenogenic receptor (β2-AR) expression are negatively correlated with the overall survival of pancreatic cancer patients. Moreover, HIF-1α expression and β2-AR expression are positively correlated with smoking status, different histological differentiation and among the tumor node metastasis (TNM) stages in pancreatic cancer patients. NNK increases HIF-1α expression in pancreatic cancer in vitro and in vivo. Furthermore, knockdown of HIF-1α and ICI118, 551 (a β2-AR selective antagonist) abrogates NNK-induced pancreatic cancer proliferation and invasion in vitro and inhibits NNK-induced pancreatic cancer growth in vivo. However, using CoCl2 (a HIF-1α stabilizing agent which decreases HIF-1α degradation under normoxia conditions) reverses ICI118, 551 induced effects under NNK exposure. Thus, our data indicate that β2-AR signaling regulates NNK-induced pancreatic cancer progression via upregulation of HIF-1α. Taken together, β2-AR signaling and HIF-1α may represent promising therapeutic targets for preventing smoking induced pancreatic cancer progression.

Published
2016
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