Jing-Yuan Fang

Shanghai Jiao Tong University, Shanghai, Shanghai Shi, China

Are you Jing-Yuan Fang?

Claim your profile

Publications (127)501.94 Total impact

  • 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.
    Journal of Digestive Diseases 08/2015; DOI:10.1111/1751-2980.12282 · 1.92 Impact Factor
  • 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.
    Scientific Reports 06/2015; 5:11763. DOI:10.1038/srep11763 · 5.58 Impact Factor
  • Hui-Min Chen · Jing-Yuan Fang
    05/2015; 1(4):201-208. DOI:10.1159/000380784
  • Ya-Nan Yu · Jing-Yuan Fang
    05/2015; 2(1):26-32. DOI:10.1159/000380892
  • Yanan Yu · Zibin Tian · Tachung Yu · Jie Hong · Jing-Yuan Fang
    Gastroenterology 04/2015; 148(4):S-371-S-372. DOI:10.1016/S0016-5085(15)31245-2 · 13.93 Impact Factor
  • Jin Qian · Jie Xu · Jing-Yuan Fang
    Gastroenterology 04/2015; 148(4):S-103-S-104. DOI:10.1016/S0016-5085(15)30357-7 · 13.93 Impact Factor
  • Tian-Tian Sun · Haoyan Chen · Jie Hong · Jing-Yuan Fang
    Gastroenterology 04/2015; 148(4):S-564. DOI:10.1016/S0016-5085(15)31900-4 · 13.93 Impact Factor
  • Lin-Lin Ren · Jie Hong · Haoyan Chen · Jing-Yuan Fang
    Gastroenterology 04/2015; 148(4):S-374. DOI:10.1016/S0016-5085(15)31255-5 · 13.93 Impact Factor
  • Jie Xu · Ye Hu · Jing-Yuan Fang
    Gastroenterology 04/2015; 148(4):S-570. DOI:10.1016/S0016-5085(15)31924-7 · 13.93 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Members of the inositol phosphate metabolism pathway regulate cell proliferation, migration and phosphatidylinositol-3-kinase (PI3K)/Akt signaling, and are frequently dysregulated in cancer. Whether germline genetic variants in inositol phosphate metabolism pathway are associated with cancer risk remains to be clarified. We examined the association between inositol phosphate metabolism pathway genes and risk of eight types of cancer using data from genome-wide association studies. Logistic regression models were applied to evaluate SNP-level associations. Gene- and pathway-based associations were tested using the permutation-based adaptive rank-truncated product method. The overall inositol phosphate metabolism pathway was significantly associated with risk of lung cancer (P = 2.00 × 10(-4)), esophageal squamous cell carcinoma (P = 5.70 × 10(-3)), gastric cancer (P = 3.03 × 10(-2)) and renal cell carcinoma (P = 1.26 × 10(-2)), but not with pancreatic cancer (P = 1.40 × 10(-1)), breast cancer (P = 3.03 × 10(-1)), prostate cancer (P = 4.51 × 10(-1)), and bladder cancer (P = 6.30 × 10(-1)). Our results provide a link between inherited variation in the overall inositol phosphate metabolism pathway and several individual genes and cancer. Further studies will be needed to validate these positive findings, and to explore its mechanisms.
    Scientific Reports 02/2015; 5:8473. DOI:10.1038/srep08473 · 5.58 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Since observational data in the urban residents are required to better assess the risk factors of colorectal neoplasm occurrence and the effectiveness of colonoscopy screening and surveillance, we conducted a case-control study at multicenters in China to identify patient characteristics and neoplasm features of colorectal adenoma (CRA) and colorectal carcinoma (CRC). A total of 4089 patients who had undergone a colonoscopy from 19 hospitals were enrolled, of which 1106 had CRA and 466 had CRC. They were compared with controls. The analysis provides features and risk factors of colorectal neoplasm using multivariate logistic regression. Increasing age, a family history of colorectal cancer or previous cases of colorectal adenoma or hypertension disease, gastrointestinal surgery, regular intake of pickled food (adjusted odds ratio [aOR] 1.42, 95 % confidence interval [CI], 1.048-1.924), consumption of alcohol, and a positive result of fecal occult blood testing (FOBT; aOR 2.509, 95 % CI 1.485-4.237) were associated with an increased risk of CRA. In the CRC group, increasing age, regular intake of pickled foods, and a positive FOBT result were risk factors. In addition, a positive abdominal computed tomography (CT) before a colonoscopy and physical signs of emaciation were also significantly associated with an increasing risk of colorectal carcinoma. Regular intake of vegetables decreased the risk of both CRA and CRC. Age, pickled foods, and a positive FOBT are risk factors for colorectal neoplasm. Vegetable intake was associated with a decreased risk of CRA and CRC.
    International Journal of Colorectal Disease 12/2014; 30(3). DOI:10.1007/s00384-014-2090-9 · 2.42 Impact Factor
  • Haoyan Chen · Jie Xu · Jie Hong · Ruqi Tang · Xi Zhang · Jing-Yuan Fang
    [Show abstract] [Hide abstract]
    ABSTRACT: Colorectal cancer (CRC) is a heterogeneous disease in terms of clinical behavior and response to therapy. Increasing evidence suggests that long noncoding RNAs (lncRNAs) are frequently aberrantly expressed in cancers, and some of them have been implicated in CRC biogenesis and prognosis. Using an lncRNA-mining approach, we constructed lncRNAs expression profiles in approximately 888 CRC samples. By applying unsupervised consensus clustering to LncRNA expression profiles, we identified five distinct molecular subtypes of CRC with different biological pathways and phenotypically distinct in their clinical outcome in both univariate and multivariate analysis. The prognostic significance of the lncRNA-based classifier was confirmed in independent patient cohorts. Further analysis revealed that most of the signature lncRNAs positively correlated with somatic copy number alterations (SCNAs). This lncRNAs-based classification schema thus provides a molecular classification applicable to individual tumors that has implications to influence treatment decisions.
    Molecular Oncology 12/2014; 8(8). DOI:10.1016/j.molonc.2014.05.010 · 5.94 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: It is increasingly evident that long non-coding RNAs (lncRNA) have causative roles in carcinogenesis. In this study, we report findings implicating a novel lncRNA in gastric cancer (GC), termed GAPLINC, based on the use of global microarray and in situ hybridization (ISH) analyses to identify aberrantly expressed lncRNA in human GC specimens. GAPLINC is a 924-bp long lncRNA that is highly expressed in GC tissues. GAPLINC suppression and with gene expression profiling in GC cells revealed alterations in cell migration pathways, with CD44 expression the most highly correlated. Manipulating GAPLINC expression altered CD44 mRNA abundance and the effects of GAPLINC on cell migration and proliferation were neutralized by suppressing CD44 expression. Mechanistic investigations revealed that GAPLINC regulates CD44 as a molecular decoy for miR211-3p, a microRNA that targets both CD44 and GAPLINC. Tissue ISH analysis suggested that GAPLINC overexpression defines a subgroup of GC patients with very poor survival. Taken together, our results identify a non-coding regulatory pathway for the CD44 oncogene, shedding new light on the basis for GC cell invasiveness.
    Cancer Research 10/2014; 74(23). DOI:10.1158/0008-5472.CAN-14-0686 · 9.28 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Recent studies have increasingly linked microRNAs to colorectal cancer (CRC). MiR-194 has been reported deregulated in different tumor types, whereas the function of miR-194 in CRC largely remains unexplored. Here we investigated the biological effects, mechanisms and clinical significance of miR-194. Functional assay revealed that overexpression of miR-194 inhibited CRC cell viability and invasion in vitro and suppressed CRC xenograft tumor growth in vivo. Conversely, block of miR-194 in APC(Min/+) mice promoted tumor growth. Furthermore, miR-194 reduced the expression of AKT2 both in vitro and in vivo. Clinically, the expression of miR-194 gradually decreased from 20 normal colorectal mucosa (N-N) cases through 40 colorectal adenomas (CRA) cases and then to 40 CRC cases, and was negatively correlated with AKT2 and pAKT2 expression. Furthermore, expression of miR-194 in stool samples was gradually decreased from 20 healthy cases, 20 CRA cases, then to 28 CRC cases. Low expression of miR-194 in CRC tissues was associated with large tumor size (P=0.006), lymph node metastasis (P=0.012) and shorter survival (HR =2.349, 95% CI = 1.242 to 4.442; P=0.009). In conclusion, our data indicated that miR-194 acted as a tumor suppressor in the colorectal carcinogenesis via targeting PDK1/AKT2/XIAP pathway, and could be a significant diagnostic and prognostic biomarker for CRC.
    Theranostics 09/2014; 4(12):1193-208. DOI:10.7150/thno.8712 · 7.83 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: In this study we investigated the biological role and mechanism of miR-198 in colorectal carcinoma (CRC). MiR-198 expression was shown to exhibit a strongly negative correlation with lymph node invasion, distant metastasis and patient survival in examinations of colorectal cancer tissues and paired normal colorectal mucosa tissues. fucosyl transferase 8 (FUT8) was identified as a potential target of miR-198 in bioinformatics analysis and luciferase reporter assays. Overexpression of miR-198 in CRC cell lines decreased FUT8 levels as shown by immunofluorescence analysis, and inhibited cell proliferation, migration, and invasion. These anti-tumor phenotypes were rescued by reconstitution of FUT8 expression. Furthermore, miR-198 was shown to target the 3'UTR of FUT8 directly to downregulate FUT8 expression at both mRNA and protein levels in qRT-PCR and Western blot analyses, respectively. In vivo, restoration of miR-198 significantly inhibited xenograft growth and invasion of CRC tumors in nude mice. Therefore, it could be concluded that miR-198 suppresses the proliferation and invasion of CRC by directly targeting FUT8.
    Scientific Reports 09/2014; 4:6145. DOI:10.1038/srep06145 · 5.58 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The impact of cellular oxidative stress in promoting the epithelial-mesenchymal transition (EMT) has been noticed. Our previous study shows that SENP3, a redox-sensitive SUMO2/3-specific protease, accumulates in a variety of cancers, but whether SENP3 and SUMOylation involve in the regulation of EMT is unclear. The present study uncovers a novel role of SENP3 in promoting the EMT process in gastric cancer via regulating an EMT-inducing transcription factor, forkhead box C2 (FOXC2). We demonstrate that the expression of mesenchymal marker genes and cell migration ability are enhanced in SENP3-overexpressing gastric cancer cells and attenuated in SENP3-knockdown cells. A nude mouse model and a set of patient's specimens suggest the correlation between SENP3 and gastric cancer metastasis. Biochemical assays identify FOXC2 as a substrate of SENP3. Meanwhile N-cadherin is verified as a target gene of FOXC2, which is transcriptionally activated by a SUMO-less FOXC2. Additionally, reactive oxygen species-induced de-SUMOylation of FOXC2 can be blocked by silencing endogenous SENP3. In conclusion, SENP3, which is increased in gastric cancer cells, potentiates the transcriptional activity of FOXC2 through de-SUMOylation, in favor of the induction of specific mesenchymal gene expression in gastric cancer metastasis.
    Oncotarget 08/2014; 5(16):7093-7104. · 6.63 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Covalent modification adding acetyl groups to the C terminus of the p53 protein has been suggested to be required for its functional activation as a tumour suppressor. However, it remains largely unknown how p53 acetylation is deregulated in colorectal cancer (CRC), which is the third most commonly diagnosed cancer worldwide. Here we show that ArhGAP30, a Rho GTPase-activating protein, is a pivotal regulator for p53 acetylation and functional activation in CRC. ArhGAP30 binds to p53 C-terminal domain and P300, facilitating P300-mediated acetylation of p53 at lysine 382. ArhGAP30 expression is required for p53 activation upon DNA damage stress, and the level of ArhGAP30 correlates with p53 acetylation and functional activation in CRC tissues. Moreover, low level of ArhGAP30 expression associates with poor survival of CRC patients. In summary, ArhGAP30 is required for p53 acetylation and functional activation in CRC, and the expression of ArhGAP30 is a potential prognostic marker for CRC.
    Nature Communications 08/2014; 5:4735. DOI:10.1038/ncomms5735 · 10.74 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Background A higher prevalence of chronic atrophic gastritis (CAG) occurs in younger adults in Asia. We used Stomach Age to examine the different mechanisms of CAG between younger adults and elderly individuals, and established a simple model of cancer risk that can be applied to CAG surveillance. Methods Stomach Age was determined by FISH examination of telomere length in stomach biopsies. Δψm was also determined by flow cytometry. Sixty volunteers were used to confirm the linear relationship between telomere length and age while 120 subjects were used to build a mathematical model by a multivariate analysis. Overall, 146 subjects were used to evaluate the validity of the model, and 1,007 subjects were used to evaluate the relationship between prognosis and Δage (calculated from the mathematical model). ROC curves were used to evaluate the relationship between prognosis and Δage and to determine the cut-off point for Δage. Results We established that a tight linear relationship between the telomere length and the age. The telomere length was obvious different between patients with and without CAG even in the same age. Δψm decreased in individuals whose Stomach Age was greater than real age, especially in younger adults. A mathematical model of Stomach Age (real age + Δage) was successfully constructed which was easy to apply in clinical work. A higher Δage was correlated with a worse outcome. The criterion of Δage >3.11 should be considered as the cut-off to select the subgroup of patients who require endoscopic surveillance. Conclusion Variation in Stomach Age between individuals of the same biological age was confirmed. Attention should be paid to those with a greater Stomach Age, especially in younger adults. The Δage in the Simple Model can be used as a criterion to select CAG patients for gastric cancer surveillance.
    BMC Clinical Pathology 06/2014; 14:29. DOI:10.1186/1472-6890-14-29
  • [Show abstract] [Hide abstract]
    ABSTRACT: Serotonin (5-HT) plays pivotal roles in the pathogenesis of post-infectious irritable bowel syndrome (PI-IBS), and luminal 5-HT time-dependently modulates visceral nociception. We found that duodenal biopsies from PI-IBS patients exhibited increased 5-HT and decreased anandamide levels and that decreased anandamide was associated with abdominal pain severity, indicating a link between 5- HT and endocannabinoid signaling pathways in PI-IBS. To understand this, we investigated the role of endocannabinoids in 5-HT modulation of visceral nociception in a rat model. Acute intraduodenally applied 5-HT attenuated the visceromotor response (VMR) to colorectal distention, and this was reversed by the cannabinoid receptor 1 (CB1) antagonist AM251. Duodenal anandamide (but not 2- arachidonoylglycerol) content was greatly increased after luminal 5-HT treatment. This effect was abrogated by the 5-HT3 receptor (5-HT3R) antagonist granisetron, which was luminally delivered to preferentially target vagal terminals. Chemical denervation of vagal afferents blocked 5-HT-evoked antinociception and anandamide release. Chronic luminal 5-HT exposure for 5 days increased baseline VMR and VMR post-5-HT (days 4 and 5). Duodenal levels of anandamide and N-acylphosphatidylethanolamine- specific phospholipase D (NAPE-PLD, the anandamide-synthesizing enzyme) protein gradually declined from day 1 to 5. The time-dependent effects of 5-HT were abolished by daily granisetron pretreatment. Daily pretreatment with CB1 agonists or anandamide from day 3 attenuated 5-HT-induced hyperalgesia. These data suggest that vagal 5-HT3R-mediated duodenal anandamide release contributes to acute luminal 5-HT-induced antinociception via CB1 signaling, whereas decreased anandamide is associated with hyperalgesia upon chronic 5-HT treatment. Further understanding of peripheral vagal anandamide signaling may provide insights into the mechanisms underlying 5-HT-related IBS.
    Pain 05/2014; 155(8). DOI:10.1016/j.pain.2014.05.005 · 5.84 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Background: Colorectal cancer (CRC) is steadily increasing in China. Colorectal adenoma (CRA) is the most important precancerous disease of CRC. Screening for colorectal tumors can aid early diagnosis. Advances in endoscopic mucosal resection and endoscopic submucosal dissection can aid the early treatment of colorectal tumors. Furthermore, because of high risk of recurrence after removal of adenomas under endoscopy, factors contributing to recurrence, the follow-up mode and the interval established, and the feasibility of application and the time of various chemical preventions should be concerned. However, a relevant consensus on the screening, early diagnosis and treatment, and prevention of colorectal tumors in China is lacking. Summary: The consensus recommendations include epidemiology, pathology, screening, early diagnosis, endoscopic treatment, monitoring and follow-up, and chemoprevention of colorectal tumors in China. Key Message: This is the first consensus on the prevention, screening, early diagnosis and treatment of CRA and CRC in China based on evidence in the literature and on local data. Practical Implications: Through reviewing the literature, regional data and passing the consensus by an anonymous vote, gastroenterology experts from all over China launch the consensus recommendations in Shanghai. The incidence and mortality of CRC in China has increased, and the incidence or detection rate of CRA has increased rapidly. Screening for colorectal tumors should be performed at age 50-74 years. Preliminary screening should be undertaken to find persons at high risk, followed by colonoscopy. A screening cycle of 3 years is recommended for persistent interventions. Opportunistic screening is a mode suitable for the current healthcare system and national situation. Colonoscopy combined with pathological examination is the standard method for the diagnosis of colorectal tumors. CRA removal under endoscopy can prevent CRC to some extent, but CRA has an obvious recurrence trend. The follow-up interval after the removal or surgery of colorectal tumors should be different with lesions. Primary prevention of CRA includes improved diet with more fiber, supplements containing calcium and vitamin D, supplements containing folic acid for those with low hemoglobin levels, and cessation of tobacco smoking. Non-steroidal anti-inflammatory drugs and selective cyclooxygenase-2 inhibitors have been recognized to prevent recurrence after adenoma removal.
    05/2014; 1(2):53-75. DOI:10.1159/000362585

Publication Stats

1k Citations
501.94 Total Impact Points

Institutions

  • 2006–2015
    • Shanghai Jiao Tong University
      • • Department of Gastroenterology and Hepatology (Renji)
      • • Institute of Digestive Disease
      • • State Key Laboratory of Oncogenes and Related Genes
      • • Renji Hospital
      Shanghai, Shanghai Shi, China
  • 2002–2014
    • Renji Hospital
      Shanghai, Shanghai Shi, China
  • 2008–2013
    • Xin Hua Hospital Affiliated to Shanghai Jiao Tong University School of Medicine
      Shanghai, Shanghai Shi, China