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Pancreatic Neoplasms: HELP
Articles by W. Li
Based on 3 articles published since 2010
(Why 3 articles?)
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Between 2010 and 2020, W. Li wrote the following 3 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article Downregulated miR-506 expression facilitates pancreatic cancer progression and chemoresistance via SPHK1/Akt/NF-κB signaling. 2016

Li, J / Wu, H / Li, W / Yin, L / Guo, S / Xu, X / Ouyang, Y / Zhao, Z / Liu, S / Tian, Y / Tian, Z / Ju, J / Ni, B / Wang, H. ·Institute of Hepatopancreatobiliary Surgery, Southwest Hospital, Third Military Medical University, Chongqing, China. · Department of Pancreatic Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. · Department of Oncology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University, Chongqing, China. · Institute of Immunology PLA, Third Military Medical University, Chongqing, China. · Translational Research Laboratory, Department of Pathology, Stony Brook University, Stony Brook, NY, USA. · Department of Pathophysiology and High Altitude Pathology, Third Military Medical University, Chongqing, China. ·Oncogene · Pubmed #27065335.

ABSTRACT: The aberrant expression of microRNAs (miRNAs) has emerged as an important hallmark of cancer. However, the molecular mechanisms underlying the changes in miRNA expression remain unclear. In this study, we discovered a novel epigenetic mechanism of miR-506 regulation and investigated its functional significance in pancreatic cancer. Sequencing analysis revealed that the miR-506 promoter is highly methylated in pancreatic cancer tissues compared with non-cancerous tissues. Reduced miR-506 expression was significantly associated with clinical stage, pathologic tumor status, distant metastasis and decreased survival of pancreatic cancer patients. miR-506 inhibited cell proliferation, induced cell cycle arrest at the G1/S transition and enhanced apoptosis and chemosensitivity of pancreatic cancer cells. Furthermore, we identified sphingosine kinase 1 (SPHK1) as a novel target of miR-506, the expression of which inhibited the SPHK1/Akt/NF-κB signaling pathway, which is activated in pancreatic cancer. High SPHK1 expression was significantly associated with poor survival in a large cohort of pancreatic cancer specimens. Our data suggest that miR-506 acts as a tumor suppressor miRNA and is epigenetically silenced in pancreatic cancer. The newly identified miR-506/SPHK1 axis represents a novel therapeutic strategy for future pancreatic cancer treatment.

2 Article miR-1247 is correlated with prognosis of pancreatic cancer and inhibits cell proliferation by targeting neuropilins. 2014

Shi, S / Lu, Y / Qin, Y / Li, W / Cheng, H / Xu, Y / Xu, J / Long, J / Liu, L / Liu, C / Yu, X. ·(X. Yu) No. 270, Dong'An Road, Xuhui District, Shanghai, 200032, P.R. China. yuxianjun@fudan.edu.cn. ·Curr Mol Med · Pubmed #24588767.

ABSTRACT: Accumulating evidence indicates that microRNAs (miRNAs) have great potential as tumor biomarkers and therapeutic agents owing to their functions in tumorigenesis and cancer progression. Aberrant expression of miR-1247 has been found in several cancers and is predicted to play an important role in the pathological processes of pancreatic cancer by miRNA-regulated network analysis. We investigated the expression profile of miR-1247 in pancreatic cancer tissue microarray by in situ hybridization and found that miR-1247 was significantly down-regulated in pancreatic cancer tissues compared to matched benign tissues. High levels of miR-1247 expression were positively correlated with higher overall and recurrence free survival in pancreatic cancer patients, while negatively correlated with tumor grade. Using in vitro and in vivo models, we demonstrated that increased expression of miR-1247 inhibited proliferation, tumorigenicity, colony formation and triggered G0/G1 cell cycle arrest in pancreatic cancer cells. Moreover, we confirmed that neuropilin1 (NRP1) and neuropilin2 (NRP2) are direct targets of miR-1247 by western blot and luciferase reporter assay. Further studies indicated that low dose all trans retinoic acid (ATRA) can induce redifferentiation and restoration of miR-1247 in pancreatic cancer cells. These findings suggest that miR-1247, a novel tumor suppressor, can act as a potential biomarker and therapeutic agent for pancreatic cancer.

3 Article β2-AR-HIF-1α: a novel regulatory axis for stress-induced pancreatic tumor growth and angiogenesis. 2013

Shan, T / Ma, J / Ma, Q / Guo, K / Guo, J / Li, X / Li, W / Liu, J / Huang, C / Wang, F / Wu, E. ·Department of Hepatobiliary Surgery, First Affiliated Hospital of Medical College, Xi'an Jiaotong University, Xi'an, Shaanxi, China. ·Curr Mol Med · Pubmed #23745588.

ABSTRACT: The purpose of this study was to test the hypothesis that chronic stress in a negative social and psychological state plays a critical role in pancreatic cancer development and progression. In this study, we created a new stress model system to determine the effects of chronic stress on pancreatic cancer progression. Here, we show that chronic stress not only causes depression in mice, most likely attributed to an elevated level of epinephrine, but also induces pancreatic cancer progression. We provide evidence that the pancreatic cancer progression induced by chronic stress could be blocked to a significant degree by β2-AR inhibitor ICI118 551 or HIF-1α inhibitor 2-methoxyestradiol. Moreover, establishment of pancreatic cancer in mice exposed to chronic stress was accompanied by up-regulation of the expression of MMP-2, MMP-9, and VEGF, mediated by a HIF- 1α-dependent β-AR signaling pathway. Our data suggest that the β2-AR-HIF-1α axis regulates stress-induced pancreatic tumor growth and angiogenesis. This study may have a therapeutic or preventive potential for the patients with pancreatic cancer who are especially prone to psychosocial stress challenges.