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Pancreatic Neoplasms: HELP
Articles by Wen-Jun Yang
Based on 4 articles published since 2010
(Why 4 articles?)
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Between 2010 and 2020, W. J. Yang wrote the following 4 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article Three novel genetic variants in NRF2 signaling pathway genes are associated with pancreatic cancer risk. 2019

Yang, Wenjun / Liu, Hongliang / Duan, Bensong / Xu, Xinyuan / Carmody, Dennis / Luo, Sheng / Walsh, Kyle M / Abbruzzese, James L / Zhang, Xuefeng / Chen, Xiaoxin / Wei, Qingyi. ·Key Laboratory of Fertility Preservation and Maintenance, School of Basic Medicine and the General Hospital, Ningxia Medical University, Yinchuan, China. · Cancer Research Program, Julius L. Chambers Biomedical Biotechnology Research Institute, North Carolina Central University, Durham. · Duke Cancer Institute, Duke University Medical Center, Durham. · Department of Population Health Sciences, Duke University School of Medicine, Durham. · Department of Biostatistics and Bioinformatics, Duke University School of Medicine, Durham. · Department of Neurosurgery, Duke University School of Medicine, Durham. · Department of Medicine, Population Health Sciences, Duke University School of Medicine, Durham. · Department of Pathology, Duke University School of Medicine, Durham. ·Cancer Sci · Pubmed #30972876.

ABSTRACT: Pancreatic cancer (PanC) is one of the most lethal solid malignancies, and metastatic PanC is often present at the time of diagnosis. Although several high- and low-penetrance genes have been implicated in PanC, their roles in carcinogenesis remain only partially elucidated. Because the nuclear factor erythroid2-related factor2 (NRF2) signaling pathway is involved in human cancers, we hypothesize that genetic variants in NRF2 pathway genes are associated with PanC risk. To test this hypothesis, we assessed associations between 31 583 common single nucleotide polymorphisms (SNP) in 164 NRF2-related genes and PanC risk using three published genome-wide association study (GWAS) datasets, which included 8474 cases and 6944 controls of European descent. We also carried out expression quantitative trait loci (eQTL) analysis to assess the genotype-phenotype correlation of the identified significant SNP using publicly available data in the 1000 Genomes Project. We found that three novel SNP (ie, rs3124761, rs17458086 and rs1630747) were significantly associated with PanC risk (P = 5.17 × 10

2 Article Restoration of miRNA-148a in pancreatic cancer reduces invasion and metastasis by inhibiting the Wnt/β-catenin signaling pathway via downregulating maternally expressed gene-3. 2019

Sun, Yunpeng / Zhu, Qiandong / Zhou, Mengtao / Yang, Wenjun / Shi, Hongqi / Shan, Yunfeng / Zhang, Qiyu / Yu, Fuxiang. ·Department of Hepatobiliary Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325015, P.R. China. ·Exp Ther Med · Pubmed #30651845.

ABSTRACT: Various microRNAs (miRNA) have been recognized potential novel tumor markers and have a critical role in cancer development and progression. Recently, methylation of miRNA-148a was identified as a crucial biochemical process in the progression of cancer. However, its potential role and in pancreatic cancer as well as the underlying mechanisms have remained largely elusive. The present study investigated the potential antitumor effect of miR-148a as well as its impact on invasion and metastasis in pancreatic cancer. It was found that the expression of miRNA-148a and the potential predictive biomarker maternally expressed gene-3 (MEG-3) were obviously decreased in human pancreatic cancer tissues compared with those in adjacent non-tumorous tissues. Furthermore, miR-148a was found to be downregulated in pancreatic cancer cell lines compared with normal pancreatic cells through promoter methylation. An MTT assay and a clonogenic assay demonstrated that restoration of miRNA-148a inhibited the proliferation and colony formation of pancreatic cancer cells. In addition, miR-148a transduction led to the upregulation of MEG-3 expression and promoted apoptosis of pancreatic cancer cells. Western blot analysis revealed that transduction of miR-148a markedly decreased the expression levels of C-myc, cyclin D1 and β-catenin in pancreatic cancer cells. Methylation of miR-148a not only decreased the endogenous β-catenin levels but also inhibited the nuclear translocation of β-catenin to delay cell cycle progression. Furthermore, ectopic miR-148a methylation inhibited pancreatic cancer cell migration and invasion via causing an upregulation of MEG-3 expression. Most importantly, ectopic overexpression of miR-148a in pancreatic cancer cells inhibited tumor formation in an animal experiment. Taken together, miR-148a methylation is a crucial regulatory process to inhibit the proliferation and invasion of pancreatic cancer cells, and transduction of miR-148a suppressed the proliferation of pancreatic cancer cells through negative regulation of the Wnt/β-catenin signaling pathway. The findings of the present study suggested that miRNA-148a acts as a tumor suppressor in pancreatic cancer and may contribute to the development of novel treatments for pancreatic cancer.

3 Article Mitochondrial tRNALeu(CUN) A12307G variant may not be associated pancreatic cancer. 2016

Li, Y / Huang, A W / Chen, Y Z / Yang, W J / Zhou, M T / Sun, H W. ·Department of Operating Room, First Affiliated Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China. · Department of Surgery, First Affiliated Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China. ·Genet Mol Res · Pubmed #27323166.

ABSTRACT: Mitochondrial DNA mutations that lead to mitochondrial dysfunction have long been proposed to play important roles in the development of pancreatic cancer. Of these, alterations to mitochondrial tRNA genes constitute the largest group. Most recently, a variation at position 12307 in the gene encoding tRNA(Leu(CUN)) has been reported to be associated with this disease. However, the molecular mechanism underlying this relationship remains poorly understood. To assess this association, we evaluated this variant by evolutionary conservation analysis, measurements of allelic frequencies among control subjects, and use of several bioinformatic tools to estimate potential structural and functional alterations. We found this residue to have a high conservation index; however, the presence of the A12307G variation in control subjects revealed by a literature search suggested it to be common in human populations. Moreover, RNAfold results showed that this variant did not alter the secondary structure of tRNA(Leu(CUN)). Through the application of a pathogenicity scoring system, this variant was determined to be a "neutral polymorphism," with a score of only 4 points based on current data. Thus, the contribution of the A12307G variant to pancreatic cancer needs to be addressed in further experimental studies.

4 Article Effect of NK4 transduction in bone marrow-derived mesenchymal stem cells on biological characteristics of pancreatic cancer cells. 2014

Sun, Yun-Peng / Zhang, Ben-Long / Duan, Jian-Wen / Wu, Huan-Huan / Wang, Ben-Quan / Yu, Zheng-Ping / Yang, Wen-Jun / Shan, Yun-Feng / Zhou, Meng-Tao / Zhang, Qi-Yu. ·Department of Hepatobiliary Surgery, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325015, Zhejiang, China. syfsjb@sina.com. · Department of General Surgery, Yiwu Chouzhou Hospital, Yiwu 322000, Zhejiang, China. zhangbenlong0021@126.com. · Department of Hepatobiliary Surgery, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325015, Zhejiang, China. djw3522@163.com. · Department of Infectious Disease, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325015, Zhejiang, China. wuhh19@sina.com. · Department of Hepatobiliary Surgery, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325015, Zhejiang, China. wangbeq@sohu.com. · Department of Hepatobiliary Surgery, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325015, Zhejiang, China. yjping45@tom.com. · Department of Hepatobiliary Surgery, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325015, Zhejiang, China. greatywj@sohu.com. · Department of Hepatobiliary Surgery, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325015, Zhejiang, China. zmtzmtao@126.com. · Department of Hepatobiliary Surgery, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325015, Zhejiang, China. zhangqiyu0123@126.com. ·Int J Mol Sci · Pubmed #24595237.

ABSTRACT: Pancreatic cancer usually has a poor prognosis, and no gene therapy has yet been developed that is effective to treat it. Since a unique characteristic of bone marrow-derived mesenchymal stem cells (MSCs) is that they migrate to tumor tissues, we wanted to determine whether MSCs could serve as a vehicle of gene therapy for targeting pancreatic cancer. First, we successfully extracted MSCs from SD rats. Next, MSCs were efficiently transduced with NK4, an antagonist of hepatocyte growth factor (HGF) which comprising the N-terminal and the subsequent four kringle domains of HGF, by an adenoviral vector. Then, we confirmed that rat MSCs preferentially migrate to pancreatic cancer cells. Last, MSCs expressing NK4 (NK4-MSCs) strongly inhibited proliferation and migration of the pancreatic cancer cell line SW1990 after co-culture. These results indicate that MSCs can serve as a vehicle of gene therapy for targeting pancreatic cancer.