Jing-Yuan Fang

Shanghai Jiao Tong University, Shanghai, Shanghai Shi, China

Are you Jing-Yuan Fang?

Claim your profile

Publications (144)627.15 Total impact

  • Yao Zhang · Ye Hu · Jing-Yuan Fang · Jie Xu
    [Show abstract] [Hide abstract]
    ABSTRACT: Missense mutation of p53 not only impairs its tumor suppression function, but also causes oncogenic gain of function (GOF). The molecular underpinning of mutant p53 (mutp53) GOF is not fully understood, especially for the potential roles of non-coding genes. Here we identify the microRNA expression profile (microRNAome) of mutp53 on Arg282 by controlled microarray experiments, and clarify the prognostic significance of mutp53-regulated miRNAs in cancers. A predominant repression effect on miRNA expression was found for mutant p53, with 183 significantly downregulated and only 12 upregulated miRNAs. Mutp53 and wild-type (wtp53) commonly upregulate let-7i, and other two miRNAs were upregulated by wtp53 but repressed by mutp53 (miR-610 and miR-3065-3p). Based the mutp53-regulated miRNA signature, a non-negative matrix factorization (NMF) model classified gastric cancer (GC) cases into subgroups with significantly different Disease-free survival (Kaplan-Meier test, P = 0.013). In contrast, the NMF model based on all miRNAs did not associate with cancer outcome. The mutp53 miRNA signature associated with the outcomes of breast cancer (P = 0.024) and hepatocellular cancer (P = 0.012). The miRPath analysis revealed that mutp53-suppressed miRNAs associate with Hippo, TGF-β and stem cell signaling pathways. Taken together, our results highlight a miRNA-mediated GOF mechanism of mutant p53 on Arg282, and suggest the prognostic potential of mutp53-associated miRNA signature.
    No preview · Article · Feb 2016 · Oncotarget
  • Zhen-Hua Wang · Jing-Yuan Fang
    [Show abstract] [Hide abstract]
    ABSTRACT: Background: Inflammatory bowel disease (IBD; including ulcerative colitis and Crohn's disease) is associated with an increased risk for colorectal cancer (CRC). Chronic mucosal inflammation is a key factor in the onset of carcinogenesis in IBD patients. Although most gene alterations that cause sporadic CRCs also occur in patients with IBD-associated CRC, some gene sequences and mutation frequencies differ between sporadic CRCs and IBD-associated CRCs. Summary: This review explores the incidence of CRC in IBD patients, with the goal of identifying the risk and protective factors for CRC in order to facilitate dysplasia management via individualized surveillance strategies. Key message: The incidence of CRC is higher among IBD patients. Identifying the risk and protective factors for CRC will facilitate dysplasia management via individualized surveillance strategies. Practical implications: Several risk factors, including active inflammation, the coexistence of primary sclerosing cholangitis, a family history of sporadic CRC and the extent and duration of colonic disease, can lead to the development of CRC in patients with IBD. These risk factors should be utilized in individualized surveillance strategies to lower CRC incidence among IBD patients. Use of 5-aminosalicylic acid may play an important role in CRC prevention. Until newer, more reliable markers of IBD-associated CRC risk are found, dysplasia will continue to be the best marker of CRC risk in IBD. Dysplasia management continues to play a key role in preventing the progression of carcinogenesis.
    No preview · Article · Dec 2015
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Several studies have been proposed to investigate the association between alcohol consumption and risk of Barrett's esophagus (BE), but as of yet, no quantitative summary of the literature to clarify the relationship between them. In our study, twenty eligible cohort studies involving 42925 participants were identified. Combined relative risk (RR) ratios for the highest versus lowest alcohol consumption levels were calculated. The alcohol dose-response analysis was performed to investigate the association between the increment consumption of 10 g/d alcohol and the risk of developing BE. Subgroup analyses were used to examine heterogeneity across the studies. A combined RR of 0.98 (0.62-1.34) was found when comparing highest vs. lowest alcohol consumption levels for BE. An inverse association between alcohol and incidence of BE (RR 0.51; 95% CI: 0.055-0.96) was demonstrated in women. Moreover, Asian drinkers had a relative higher risk of BE (RR 1.34; 95% CI: 1.11-1.56) compared with Western drinkers. In conclusion, our results showed that overall alcohol consumption was not associated with increased BE incidence. The limited data available on alcohol consumption supports a tentative inversion of alcohol consumption with BE risk in women, while Asian drinkers tend to have a higher risk of BE.
    Preview · Article · Nov 2015 · Scientific Reports
  • Source
    Jie-Ting Tang · Zhen-Hua Wang · Jing-Yuan Fang
    [Show abstract] [Hide abstract]
    ABSTRACT: Background and aims: Long interspersed element-1 (LINE-1) hypomethylation may play an important role in colorectal cancer (CRC). Studies were identified that investigated LINE-1 methylation levels in CRC compared with normal controls. Methods: The random-effects model was used to estimate standardized mean difference with 95% confidence intervals according to the heterogeneity between the studies. We explored the relationship between LINE-1 hypomethylation and microsatellite instability (MSI) status, clinical features, and molecular features in CRC patients using a fixed-effects model. Results: A total of 7396 CRC patients were included in the meta-analysis. LINE-1 methylation was significantly lower in CRC patients than in controls (P=0.000). Mean LINE-1 methylation was significantly lower in non-MSI-high than in MSI-high tumors (P=0.000). LINE-1 hypomethylation was found more frequently in patients with a family history compared with those without family history (P=0.002). Patients with left colon cancer had lower LINE-1 methylation than those with right colon cancer (P=0.001). LINE-1 methylation was not associated with body mass index or patient sex. LINE-1 hypomethylation was found in p21 lost tumors (P=0.000). LINE-1 methylation levels were not associated with KRAS or PIK3CA-mutation status. Conclusion: LINE-1 hypomethylation is a potential biomarker for risk of CRC and associated with various clinical and molecular features of CRC.
    Preview · Article · Nov 2015 · OncoTargets and Therapy
  • [Show abstract] [Hide abstract]
    ABSTRACT: Early diagnosis and treatment in pancreatic ductal adenocarcinoma (PDAC) is still a challenge worldwide. The poor survival of PDAC patients mainly due to early metastasis when first diagnosed and lack of prognostic biomarker. Ribosomal protein L15 (RPL15), an RNA-binding protein, is a component of ribosomal 60S subunit. It was reported that RPL15 is dysregulated in various type of cancers. However, little is known about the role of RPL15 in PDAC carcinogenesis and progression. Herein, we clarified RPL15 expression status may serve as an independent prognostic biomarker in three independent PDAC patient cohorts. We found that RPL15 was dramatically decreased in PDAC tissues and cell lines. The high expression of RPL15 was inversely correlated with TNM stage, histological differentiation, T classification and vascular invasion. Low expression of RPL15 was significantly associated with poor overall survival of PDAC patients. Furthermore, we demonstrated that the reduction of RPL15 may promote invasion ability of pancreatic cell by inducing EMT process. In conclusion, decreased RPL15 expression is associated with invasiveness of PDAC cells, and RPL15 expression status may serve as a reliable prognostic biomarker in PDAC patients.
    No preview · Article · Oct 2015 · Oncotarget
  • Wan Du · Jing-Yuan Fang
    [Show abstract] [Hide abstract]
    ABSTRACT: Background: Colorectal cancer is a commonly diagnosed cancer and the cause of many cancer deaths worldwide. Nutrients might be crucial in the pathogenesis and development of colorectal cancer. Although a number of studies have demonstrated the potential effects of nutrients, many challenges still remain. Summary: A tremendous amount of research has emerged concerning the roles of nutrients in colorectal cancer during the past decades. Here, we review the latest research progress on nutrients, including vitamins, folic acid, calcium, selenium and dietary fiber, involved in colorectal cancer prevention. Key Message: Nutrients are commonly consumed in foods or dietary supplements. It is clear that nutrients could play an important role and influence colorectal cancer outcomes. The relationship between nutrients and colorectal risk is complex. Vitamins, folic acid, calcium, selenium and dietary fiber have been proposed as potential agents to prevent colorectal cancer. However, some studies found that these nutrients did not reduce the incidence of colorectal cancer. Practical Implications: The supplementary dose of nutrients, the length of time required to observe the effects and confounding factors during the study might influence the role of nutrients in the prevention of colorectal cancer. Therefore, more evidence from ongoing clinical trials with different population groups and longer follow-up periods is critical to determine the relationship between nutrients and colorectal cancer.
    No preview · Article · Oct 2015
  • Ye Hu · Haiying Tian · Jie Xu · Jing-Yuan Fang
    [Show abstract] [Hide abstract]
    ABSTRACT: Long noncoding RNA (lncRNA) is >200 nucleotides long and lacks coding ability. LncRNA was regarded as transcript noise, until emerging results showed its roles in development, homeostasis and carcinogenesis. LncRNAs containing microRNA (miRNA) response elements could compete with the miRNA target gene and regulate its expression through decreasing free functional miRNA. Such lncRNA is called competing endogenous RNA (ceRNA), and the ‘lncRNA–miRNA’ interaction appreciably enriches the world of RNA–RNA regulation. Gastric cancer involves dysregulation of both protein-coding genes and noncoding genes, and the ceRNA regulatory mechanism may participate in this pathogenic process. In this review, we discuss recent findings on the roles of ceRNAs in gastric carcinogenesis.
    No preview · Article · Sep 2015 · Briefings in functional genomics
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Background: Accumulating evidence links colorectal cancer (CRC) with the intestinal microbiota. However, the disturbance of intestinal microbiota and the role of Fusobacterium nucleatum during the colorectal adenoma-carcinoma sequence have not yet been evaluated. Methods: 454 FLX pyrosequencing was used to evaluate the disturbance of intestinal microbiota during the adenoma-carcinoma sequence pathway of CRC. Intestinal microbiota and mucosa tumor-immune cytokines were detected in mice after introducing 1,2-dimethylhydrazine (DMH), F. nucleatum or Berberine (BBR), using pyrosequencing and Bio-Plex Pro™ cytokine assays, respectively. Protein expressions were detected by western blotting. Results: The levels of opportunistic pathogens, such as Fusobacterium, Streptococcus and Enterococcus spp. gradually increased during the colorectal adenoma-carcinoma sequence in human fecal and mucosal samples. F. nucleatum treatment significantly altered lumen microbial structures, with increased Tenericutes and Verrucomicrobia (opportunistic pathogens) (P < 0.05 = in wild-type C57BL/6 and mice with DMH treatment). BBR intervention reversed the F. nucleatum-mediated increase in opportunistic pathogens, and the secretion of IL-21/22/31, CD40L and the expression of p-STAT3, p-STAT5 and p-ERK1/2 in mice, compared with mice fed with F. nucleatum alone. Conclusions: F. nucleatum colonization in the intestine may prompt colorectal tumorigenesis. BBR could rescue F. nucleatum-induced colorectal tumorigenesis by modulating the tumor microenvironment and blocking the activation of tumorigenesis-related pathways.
    Preview · Article · Sep 2015 · Oncotarget
  • [Show abstract] [Hide abstract]
    ABSTRACT: Aims: To investigate the antitumor effects of probiotics Clostridium butyricum and Bacillus subtilis on colorectal cancer (CRC) progression. Materials & methods: The effects of C. butyricum and B. subtilis on CRC cells were studied. Male C57BL/6 mice with 1,2-dimethylhydrazine dihydrochloride (DMH)-induced CRC were intervened by these two probiotics and the antitumor effects were examined by comparing the tumor incidence and detecting the inflammatory and immune-related markers. Results & conclusions: C. butyricum and B. subtilis inhibited the proliferation of CRC cells, caused cell cycle arrest and promoted apoptosis. In vivo, these two probiotics inhibited the development of DMH-induced CRC. The molecular mechanism involved reduced inflammation and improved immune homeostasis. This work establishes a basis for the protective role of probiotics B. subtilis and C. butyricum in intestinal tumorigenesis.
    No preview · Article · Sep 2015 · Future Microbiology
  • Qin-Yan Gao · Jing-Yuan Fang
    [Show abstract] [Hide abstract]
    ABSTRACT: In China, the incidence of esophageal cancer (EC) and its related mortality are high. Screening strategies aiming at early diagnosis can improve the prognosis. Researches on detection of early EC, especially in China are reviewed. Compared to esophageal balloon cytology or routine endoscopy, chromoendoscopy with Lugol's staining and biopsy appears to be the gold standard for early EC diagnosis in China today. Narrow-band imaging endoscopy, Confocal Laser endomicroscopy and other novel diagnostic approaches are more and more widely used in developed urban areas, but cost and lack of essential training to the endoscopists have made their use limited in rural areas. No specific biomarkers or serum markers were strongly commended to be used in screening strategies currently, which need to be evaluated in future. Trials on organized screening have been proposed in some regions of china with high disease prevalence. Screening in these areas has been shown to be cost effective.
    No preview · Article · Sep 2015 · Best practice & research. Clinical gastroenterology
  • Ping Chen · Yun Cui · Qing-Yan Fu · You-Yong Lu · Jing-Yuan Fang · Xiao-Yu Chen
    [Show abstract] [Hide abstract]
    ABSTRACT: Gastric cancer is a typical type of inflammation-related tumor. p42.3 gene highly expresses in gastric cancer but whether it is associated with gastritis is still unknown. Here we will explore the relationship between inflammation and p42.3 gene. Normal gastric epithelium cells (GES-1) were treated with H. pylori and tumor necrosis factor alpha (TNF-α) separately. Total cell mRNA and protein were collected and PCR and western blotting were conducted to determine the relative expression of p42.3 gene. 291 chronic non-atrophic gastritis tissue samples were collected and immunohistochemistry method was used to measure the rate of p42.3 protein expression. The associations between p42.3 protein and the clinicopathological characteristics of patients with chronic non-atrophic gastritis were analyzed. H. pylori can significantly enhance the p42.3 protein expression in GES-1 cells. Moreover, inflammatory cytokines TNF-α can stimulate the p42.3 gene expression in GES-1 cells and further the effect showed a time and dose dependent manner. In addition, the p42.3 gene expression was positively associated with the gastric mucosa inflammation degree and H. pylori infection (P = 0.000). Its expression rate was significantly high in gastric mucosa with severe inflammation and in H. pylori infection cases. The p42.3 gene expression is associated with the gastric mucosa inflammation and it can be stimulated by TNF-α and H. pylori respectively. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.
    No preview · Article · Aug 2015 · Journal of Digestive Diseases
  • Lin-lin Ren · Hao-Yan Chen · Jie Hong · Jing-Yuan Fang

    No preview · Article · Jul 2015 · Clinical Gastroenterology and Hepatology
  • Source
    Lunxi Liang · Luoyan Ai · Jin Qian · Jing-Yuan Fang · Jie Xu
    [Show abstract] [Hide abstract]
    ABSTRACT: The gut microbiota is commonly referred to as a hidden organ due to its pivotal effects on host physiology, metabolism, nutrition and immunity. The gut microbes may be shaped by environmental and host genetic factors, and previous studies have focused on the roles of protein-coding genes. Here we show a link between long non-coding RNA (lncRNA) expression and gut microbes. By repurposing exon microarrays and comparing the lncRNA expression profiles between germ-free, conventional and different gnotobiotic mice, we revealed subgroups of lncRNAs that were specifically enriched in each condition. A nearest shrunken centroid methodology was applied to obtain lncRNA-based signatures to identify mice in different conditions. The lncRNA-based prediction model successfully identified different gnotobiotic mice from conventional and germ-free mice, and also discriminated mice harboring transplanted microbes from fecal samples of mice or zebra fishes. To achieve optimal prediction accuracy, fewer lncRNAs were required in the prediction model than protein-coding genes. Taken together, our study demonstrated the effecacy of lncRNA expression profiles in discriminating the types of microbes in the gut. These results also provide a resource of gut microbe-associated lncRNAs for the development of lncRNA biomarkers and the identification of functional lncRNAs in host-microbes interactions.
    Preview · Article · Jun 2015 · Scientific Reports
  • Hui-Min Chen · Jing-Yuan Fang
    [Show abstract] [Hide abstract]
    ABSTRACT: Background: Gastric cancer and colorectal cancer, the two most frequent cancers within the gastrointestinal tract, account for a large proportion of human malignancies worldwide. The initiation and progression of gastrointestinal cancer (GIC) is controlled by both genetic and epigenetic events. Epigenetic alterations, including changes in DNA methylation, specific histone modifications, chromatin remodeling and noncoding RNA-mediated gene silencing, are potentially reversible and heritable. Summary: In this article, we summarize the current advances in epigenetic biomarkers as potential substrates for GIC detection. The combined screening of a panel of methylated genes, hyperacetylated histones, microRNAs or other noncoding RNAs is currently under evaluation to improve sensitivity. Key message: Current studies concentrated on the development of cost-effective epigenetic diagnostic biomarkers for GIC based on noninvasive blood or stool samples. The combined blood or stool test with a relatively high sensitivity could be a cost-effective screening tool for the detection of patients with asymptomatic cancers who could therefore choose whether or not to go for further examinations, such as endoscopy or colonoscopy. Practical implications: A better understanding of epigenetic mechanisms has not only offered new insights into a deeper understanding of the underlying mechanisms of carcinogenesis, but has also allowed identification of clinically relevant putative biomarkers for the early detection, disease monitoring, prognosis and risk assessment of GIC. In particular, noninvasive biomarkers in serum or fecal samples for the detection of GIC could have potential for better compliance and can be incorporated into routine clinical practice in the foreseeable future, pending their validation in large-scale prospective trials.
    No preview · Article · May 2015
  • Ya-Nan Yu · Jing-Yuan Fang
    [Show abstract] [Hide abstract]
    ABSTRACT: Background: Colorectal cancer (CRC) is a leading cause of cancer-related mortality worldwide whose incidence has increased rapidly in recent years. There is growing evidence that the complex gut microbiota community plays an important role in the development of intestinal tumorigenesis. Summary: This review aimed to explore the correlation between gut microbiota and CRC as well as to identify the pathogens and their metabolites that affect CRC and the potential models of gut microbiota action. It promotes our understanding of the correlation between gut microbiota and CRC. Key message: Our knowledge of the risk factors associated with gut microbiota for CRC development, as well as of the mechanism how intestinal bacteria act on colorectal tumorigenesis, has improved, leading to a better understanding of the correlation between gut microbiota and CRC. Practical implications: The intestinal microbiota community has a close relationship with CRC by influencing the mechanism of the body and by regulating the physiological function of the colorectum and even the entire digestive system. Gut microbiota have been linked to CRC based upon their toxic and genotoxic metabolites production by fermentation of dietary ingredients. These metabolites could bind specific intestinal cell surface receptors and subsequently affect intracellular signal transduction. The mechanisms by which gut microbiota affect CRC development include the 'Alpha-bug' model, the 'driver-passenger' model and the 'intestinal microbiota adaptions' model. This review promotes our understanding of the correlation between gut microbiota and CRC.
    No preview · Article · May 2015
  • Jin Qian · Jie Xu · Jing-Yuan Fang

    No preview · Article · Apr 2015 · Gastroenterology
  • Yanan Yu · Zibin Tian · Tachung Yu · Jie Hong · Jing-Yuan Fang

    No preview · Article · Apr 2015 · Gastroenterology
  • Lin-Lin Ren · Jie Hong · Haoyan Chen · Jing-Yuan Fang

    No preview · Article · Apr 2015 · Gastroenterology
  • Tian-Tian Sun · Haoyan Chen · Jie Hong · Jing-Yuan Fang

    No preview · Article · Apr 2015 · Gastroenterology
  • Jie Xu · Ye Hu · Jing-Yuan Fang

    No preview · Article · Apr 2015 · Gastroenterology

Publication Stats

2k Citations
627.15 Total Impact Points

Institutions

  • 2008-2015
    • Shanghai Jiao Tong University
      • • State Key Laboratory of Oncogenes and Related Genes
      • • Institute of Digestive Disease
      • • Renji Hospital
      Shanghai, Shanghai Shi, China
  • 2002-2014
    • Renji Hospital
      Shanghai, Shanghai Shi, China
  • 2009-2013
    • Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine
      Shanghai, Shanghai Shi, China
  • 2004
    • Shanghai Medical University
      Shanghai, Shanghai Shi, China