Pick Topic
Review Topic
List Experts
Examine Expert
Save Expert
  Site Guide ··   
Pancreatic Neoplasms: HELP
Articles by Jing Xu
Based on 9 articles published since 2010
(Why 9 articles?)

Between 2010 and 2020, Jing Xu wrote the following 9 articles about Pancreatic Neoplasms.
+ Citations + Abstracts
1 Article Overexpression of GP73 promotes cell invasion, migration and metastasis by inducing epithelial-mesenchymal transition in pancreatic cancer. 2018

Song, Yin-Xue / Xu, Zhi-Chao / Li, Hui-Ling / Yang, Pei-Lei / Du, Jun-Kai / Xu, Jing. ·Department of Emergency, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, PR China. · Department of Emergency, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, PR China. Electronic address: xujingxx_jj@126.com. ·Pancreatology · Pubmed #30217697.

ABSTRACT: Pancreatic cancer is one of the most difficult clinical cases to diagnose with a very low 5-year survival rate of 5%, regardless of the advances made in both the medical and surgical treatment of the disease. One of the contributing factors for the high mortality rate seen of pancreatic cancer patients is the lack of effective chemotherapies, which is believed to be due to drug-resistance. Based on recent evidence, epithelial-mesenchymal transition (ETM) of pancreatic cancer cells has been found to be associated with the development of drug resistance and an increase in cell invasion. Therefore, we conducted the present study in order to investigate the regulatory effects of Golgi protein-73 (GP73) on PC. GP73 and EMT-related gene expressions in PC, along with the adjacent and chronic pancreatitis tissues were determined by means of RT-qPCR and Western blot analysis. Cultured PC cells were treated with pAdTrack-CMV, si-NC, GP73 overexpression, Si-GP73, Snail-siRNA and GP73 + Snail-siRNA. Cell invasion, migration and metastasis were measured in vitro and in vivo. The results revealed that the PC tissues and chronic pancreatitis tissues exhibited diminished E-cadherin expression and amplified GP73, N-cadherin, Vimentin and Snail expression. In response to GP73 gene silencing, PC cells presented with increased E-cadherin expression and decreased N-cadherin, Vimentin, Snail expression in addition to the inhibition of the number of invasive cells, tumor volume and number of liver lesions. These findings highly indicated that the overexpression of GP73 promotes cell invasion, migration and metastasis by inducing EMT in PC.

2 Article Genome-wide RNA-Seq identifies Fas/FasL-mediated tumoricidal activity of embryonic stem cells. 2018

Li, Yatong / Fan, Yongna / Xu, Jing / Zhang, Peng / Jiang, Taijiao / Dai, Menghua / Li, Limin. ·Department of General Surgery, Peking Union Medical College Hospital, Beijing, 100730, China. · State Key Laboratory of Medical Molecular Biology, Department of Pathology and Pathophysiology, Peking Union Medical College, Institute of Basic Medical Sciences, and Center of Molecular Pathology, Chinese Academy of Medical Sciences, Beijing, 100005, China. · Center for Translational Medicine, Peking Union Medical College Hospital, Peking Union Medical College & Chinese Academy of Medical Sciences, Beijing, 100730, China. · Key Laboratory of Protein and Peptide Pharmaceuticals, Institute of Biophysics, Chinese Academy of Sciences, Beijing, 100101, China. ·Int J Cancer · Pubmed #29218706.

ABSTRACT: The discovery of tumor tropism of stem cells revealed the intimate relationship between stem cells and tumor cells, but the functional role of stem cells in tumorigenesis is poorly understood. To investigate embryonic stem cell (ESC) and tumor cell interactions, we co-cultured mouse ESCs with mouse melanoma B16-F10 cells or mouse pancreatic tumor Pan02 cells, and found that ESCs significantly inhibited tumor cell proliferation. Coculture of ESCs and tumor cells resulted in significant inhibition of tumorigenesis in vivo. Histological analyses indicated that ESCs encircled apoptotic tumor cells. We carried out time course RNA-Seq analyses of ESC and tumor cell co-cultures, and identified Fas/FasL signaling as a major pathway involved in ESC-mediated apoptosis of tumor cells. We further generated FADD-deficient tumor cells by CRISPR/Cas9-mediated gene editing, and demonstrated that FADD-deficient tumor cells were obviously resistant to ESC-mediated inhibition of tumor cell proliferation. Our results indicate the Fas/FasL signaling pathway plays a critical role in ESCs-mediated tumoricidal activity.

3 Article MicroRNA-195 inhibits the proliferation and invasion of pancreatic cancer cells by targeting the fatty acid synthase/Wnt signaling pathway. 2017

Xu, Zhichao / Li, Chunli / Qu, Hui / Li, Huiling / Gu, Qiaoyan / Xu, Jing. ·1 Department of Emergency, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, P.R. China. · 2 Department of Medical Oncology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, P.R. China. · 3 Department of Gastroenterology, The Affiliated Hospital of Yan'an University, Yan'an, P.R. China. ·Tumour Biol · Pubmed #28639885.

ABSTRACT: Emerging evidence suggests that microRNAs are critical regulators of cancer development and progression. MicroRNA-195 has been reported as a cancer-related microRNA in many human cancers. However, the role of microRNA-195 in pancreatic cancer remains largely unknown. Here, we show that microRNA-195 is downregulated in pancreatic cancer tissues and cell line. Also, we show that overexpression of microRNA-195 inhibits the proliferation and invasion of pancreatic cancer cells, whereas suppression of microRNA-195 promotes proliferation and invasion. We show that microRNA-195 directly targets the fatty acid synthase enzyme and negatively regulates the expression of fatty acid synthase. Also, we show that fatty acid synthase expression is inversely correlated with microRNA-195 expression in pancreatic cancer tissues. Moreover, our results show that microRNA-195 inhibits Wnt signaling in pancreatic cancer cells. By restoring fatty acid synthase expression, we were able to reverse the antitumor effects of microRNA-195 in pancreatic cancer cells. Taken together, our findings show that microRNA-195 inhibits pancreatic cancer cell proliferation and invasion by regulating the fatty acid synthase/Wnt signaling pathway, suggesting a tumor suppressive role for microRNA-195 in the development and progression of pancreatic cancer. Thus, inhibiting fatty acid synthase by microRNA-195 may serve as a novel therapeutic approach for the treatment of pancreatic cancer.

4 Article Senescent Carcinoma-Associated Fibroblasts Upregulate IL8 to Enhance Prometastatic Phenotypes. 2017

Wang, Tao / Notta, Faiyaz / Navab, Roya / Joseph, Joella / Ibrahimov, Emin / Xu, Jing / Zhu, Chang-Qi / Borgida, Ayelet / Gallinger, Steven / Tsao, Ming-Sound. ·Princess Margaret Cancer Centre, University Health Network, Toronto, Canada. · Department of Pathology, University Health Network, Toronto, Canada. · Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Canada. · Ontario Institute for Cancer Research, Toronto, Canada. · Zane Cohen Centre for Digestive Diseases, Mount Sinai Hospital, Toronto, Canada. · Department of General Surgery, University Health Network, Toronto, Canada. · Department of Surgery, University of Toronto, Toronto, Canada. · Princess Margaret Cancer Centre, University Health Network, Toronto, Canada. ming.tsao@uhn.ca. ·Mol Cancer Res · Pubmed #27678171.

ABSTRACT: Carcinoma-associated fibroblasts (CAF) represent a significant component of pancreatic cancer stroma and are biologically implicated in tumor progression. However, evidence of both cancer-promoting and -restraining properties amongst CAFs suggests the possibility of multiple phenotypic subtypes. Here, it is demonstrated that senescent CAFs promote pancreatic cancer invasion and metastasis compared with nonsenescent control CAFs using in vitro Transwell invasion models and in vivo xenograft mouse models. Screening by gene expression microarray and cytokine ELISA assays revealed IL8 to be upregulated in senescent CAFs. Experimental modulation through IL8 overexpression or receptor inhibition implicates the IL8 pathway as a mediator of the proinvasive effects of senescent CAFs. In a cohort of human pancreatic cancer cases, more abundant stromal senescence as indicated by p16 immunohistochemistry correlated with decreased survival in patients with early-stage disease. These data support senescent fibroblasts as a pathologically and clinically relevant feature of pancreatic cancer. The inhibition of senescent stroma-cancer signaling pathways has the potential to restrain pancreatic cancer progression. IMPLICATIONS: Findings show that senescent cancer-associated fibroblasts secret excess IL8 to promote pancreatic cancer invasion and metastasis; thus, senescent CAFs represent a phenotypic subtype, challenging conventional assumptions that CAFs are a homogeneous population. Mol Cancer Res; 15(1); 3-14. ©2016 AACR.

5 Article EGFR-targeted gelatin nanoparticles for systemic administration of gemcitabine in an orthotopic pancreatic cancer model. 2016

Singh, Amit / Xu, Jing / Mattheolabakis, George / Amiji, Mansoor. ·Department of Pharmaceutical Sciences, School of Pharmacy, Northeastern University, Boston, MA, USA. · Department of Pharmaceutical Sciences, School of Pharmacy, Northeastern University, Boston, MA, USA. Electronic address: m.amiji@neu.edu. ·Nanomedicine · Pubmed #26656632.

ABSTRACT: FROM THE CLINICAL EDITOR: The treatment of pancreatic cancer remains unsatisfactory, with an average 5-year survival of less than 5%. New treatment modalities are thus urgently needed. In this study, the authors presented their formulation of redox-responsive epidermal growth factor receptor (EGFR)-targeted type B gelatin nanoparticles as a carrier for gemcitabine. In-vitro and in-vivo experiments showed encouraging results. It is hoped that the findings would provide a novel and alternative drug delivery platform for the future.

6 Article Redox-responsive targeted gelatin nanoparticles for delivery of combination wt-p53 expressing plasmid DNA and gemcitabine in the treatment of pancreatic cancer. 2014

Xu, Jing / Singh, Amit / Amiji, Mansoor M. ·Department of Pharmaceutical Sciences, School of Pharmacy, Northeastern University, 360 Huntington Avenue, Boston, MA 02115, USA. m.amiji@neu.edu. ·BMC Cancer · Pubmed #24507760.

ABSTRACT: BACKGROUND: Pancreatic adenocarcinoma is one of the most dreaded cancers with very low survival rate and poor prognosis to the existing frontline chemotherapeutic drugs. Gene therapy in combination with a cytotoxic agent could be a promising approach to circumvent the limitations of previously attempted therapeutic interventions. METHOD: We have developed a redox-responsive thiolated gelatin based nanoparticle system that efficiently delivers its payload in the presence of glutathione-mediated reducing intra-cellular environment and could be successfully used for site-specific wt-p53 expressing plasmid DNA as well as gemcitabine delivery by targeting epidermal growth factor receptor (EGFR). Efficacy studies were performed in subcutaneous human adenocarcinoma bearing SCID beige mice along with molecular level p53 plasmid and apoptotic marker expression by PCR and western blot for all study groups. RESULTS: Efficacy studies demonstrate an improved in vivo targeting efficiency resulting in increased transfection efficiency and tumor growth suppression. In all the treatment groups, the targeted nanoparticles showed better anti-tumor activity than their non-targeted as well as non-encapsulated, naked therapeutic agent counterparts (50.1, 61.7 and 77.3% tumor regression by p53 plasmid alone, gemcitabine alone and in combination respectively). Molecular analysis revealed a higher mRNA expression of transfected p53 gene, its corresponding protein and that the tumor cell death in all treatment groups was due to the induction of apoptotic pathways. CONCLUSIONS: Gene/drug combination treatment significantly improves the therapeutic performance of the delivery system compared to the gene or drug alone treated groups. Anti-tumor activity of the thiolated gelatin loaded wt-p53 plasmid or gemcitabine-based therapy was attributed to their ability to induce cell apoptosis, which was confirmed by a marked increase in mRNA level of proapoptotic transcription factors, as well as, protein apoptotic biomarker expression and significant decrease in the anti-apoptotic transcription factors.

7 Article Biodistribution and pharmacokinetics of EGFR-targeted thiolated gelatin nanoparticles following systemic administration in pancreatic tumor-bearing mice. 2013

Xu, Jing / Gattacceca, Florence / Amiji, Mansoor. ·Department of Pharmaceutical Sciences, School of Pharmacy, Northeastern University, 360 Huntington Ave, Boston, Massachusetts 02115, United States. ·Mol Pharm · Pubmed #23544877.

ABSTRACT: The objective of this study was to evaluate qualitative and quantitative biodistribution of epidermal growth factor receptor (EGFR)-targeted thiolated type B gelatin nanoparticles in vivo in subcutaneous human pancreatic adenocarcinoma (Panc-1) bearing female SCID Beige mice. EGFR-targeted nanoparticles showed preferential and sustained accumulation in the tumor mass, especially at early time points. Higher blood concentrations and higher tumor accumulations were observed with PEG-modified and EGFR-targeted nanoparticles during the study (AUClast: 17.38 and 19.56%ID/mL·h in blood, 187 and 322%ID/g·h in tumor for PEG-modified and EGFR-targeted nanoparticles, respectively), as compared to control, unmodified particles (AUClast: 10.71%ID/mL·h in blood and 138%ID/g·h in tumor). EGFR-targeted nanoparticles displayed almost twice tumor targeting efficiency than either PEG-modified or the unmodified nanoparticles, highlighting the efficacy of the active targeting strategy. In conclusion, this study shows that EGFR-targeted and PEG-modified nanoparticles were suitable vehicles for specific systemic delivery in subcutaneous Panc-1 tumor xenograft models.

8 Article Hepatitis B virus status and the risk of pancreatic cancer: a meta-analysis. 2013

Wang, Yunxia / Yang, Shengli / Song, Fujian / Cao, Shiyi / Yin, Xiaoxv / Xie, Jun / Tu, Xiaochen / Xu, Jing / Xu, Xing / Dong, Xiaoxin / Lu, Zuxun. ·Department of Social Medicine and Health Management, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China. ·Eur J Cancer Prev · Pubmed #23165286.

ABSTRACT: OBJECTIVE: Whether hepatitis B virus (HBV) infection increases the risk of pancreatic cancer (PaC) is controversial. We carried out a meta-analysis to evaluate the association between HBV status and the risk of PaC. METHODS: PubMed, Embase, and the China National Knowledge Infrastructure were searched from their inception through April 2012 for case-control and cohort studies that have reported an association between HBV status and the risk of PaC. The reference lists of pertinent publications were also reviewed for potential studies. Methodological quality was assessed using the Newcastle-Ottawa Quality Assessment Scale. A random-effects model was used to summarize odd ratios (ORs) and 95% confidence intervals (CIs). RESULTS: We included seven case-control studies and three cohort studies, involving 5883 PaC cases. The summary OR of developing PaC was 1.22 (95% CI: 0.90-1.67) for individuals who were HBV surface antigen (HBsAg)-positive. Compared with the individuals who were never exposed to HBV infection, the summary OR of the risk of PaC was 1.60 (95% CI: 1.26-2.05) for chronic or inactive HBsAg carriers (HBsAg-positive) and 1.76 (95% CI: 1.05-2.93) for anti-HBc-positive but anti-HBs-negative individuals. CONCLUSION: Inactive HBsAg carrier status and possible occult HBV infection may increase the risk of PaC. Large population-based multicenter prospective studies are required to further confirm this finding.

9 Article Therapeutic gene delivery and transfection in human pancreatic cancer cells using epidermal growth factor receptor-targeted gelatin nanoparticles. 2012

Xu, Jing / Amiji, Mansoor. ·Department of Pharmaceutical Sciences, School of Pharmacy, Northeastern University, USA. ·J Vis Exp · Pubmed #22231028.

ABSTRACT: More than 32,000 patients are diagnosed with pancreatic cancer in the United States per year and the disease is associated with very high mortality (1). Urgent need exists to develop novel clinically-translatable therapeutic strategies that can improve on the dismal survival statistics of pancreatic cancer patients. Although gene therapy in cancer has shown a tremendous promise, the major challenge is in the development of safe and effective delivery system, which can lead to sustained transgene expression. Gelatin is one of the most versatile natural biopolymer, widely used in food and pharmaceutical products. Previous studies from our laboratory have shown that type B gelatin could physical encapsulate DNA, which preserved the supercoiled structure of the plasmid and improved transfection efficiency upon intracellular delivery. By thiolation of gelatin, the sulfhydryl groups could be introduced into the polymer and would form disulfide bond within nanoparticles, which stabilizes the whole complex and once disulfide bond is broken due to the presence of glutathione in cytosol, payload would be released (2-5). Poly(ethylene glycol) (PEG)-modified GENS, when administered into the systemic circulation, provides long-circulation times and preferentially targets to the tumor mass due to the hyper-permeability of the neovasculature by the enhanced permeability and retention effect (6). Studies have shown over-expression of the epidermal growth factor receptor (EGFR) on Panc-1 human pancreatic adenocarcinoma cells (7). In order to actively target pancreatic cancer cell line, EGFR specific peptide was conjugated on the particle surface through a PEG spacer.(8) Most anti-tumor gene therapies are focused on administration of the tumor suppressor genes, such as wild-type p53 (wt-p53), to restore the pro-apoptotic function in the cells (9). The p53 mechanism functions as a critical signaling pathway in cell growth, which regulates apoptosis, cell cycle arrest, metabolism and other processes (10). In pancreatic cancer, most cells have mutations in p53 protein, causing the loss of apoptotic activity. With the introduction of wt-p53, the apoptosis could be repaired and further triggers cell death in cancer cells (11). Based on the above rationale, we have designed EGFR targeting peptide-modified thiolated gelatin nanoparticles for wt-p53 gene delivery and evaluated delivery efficiency and transfection in Panc-1 cells.