Weifeng Tang

Dr. Weifeng Tang


Research Focus & Metrics

Academic Career Length

13Years (2014-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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20 February 2017 in Oncotarget
Verified
Journal Article
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YWYafeng Wang
Yafeng Wang
QHQiuyu Huang
Qiuyu Huang
JLJianchao Liu
Jianchao Liu
YWYanan Wang
Yanan Wang
GZGongfeng Zheng
Gongfeng Zheng
ZHZiyang Huang
Ziyang Huang
Coronary heart disease (CHD) is a common complex disease resulting from the interaction of multiple environmental and genetic factors. To assess the potential relationship of vascular endothelial growth factor (VEGFA) rs699947 C>A, rs3025039 C>T and rs2010963 G>C polymorphisms with CHD risk, a comprehensive meta-analysis was conducted. A systematic search of EMBASE and PubMed online database for publications on VEGFA polymorphisms and risk of CHD was carried out. Crude Odds ratios (ORs) with their 95% confidence intervals (CIs) were calculated to determine the association. A total of ten publications including 22 trails involving 2097 cases and 2867 controls were included in our pooled analysis. Overall, results of the present meta-analysis demonstrated a significant association between VEGFA rs699947 C>A polymorphism and an increased risk of CHD. After stratifying by ethnicity and CHD type, the association was also obtained. A significant association between VEGFA rs3025039 C>T polymorphism and risk of CHD was also found. For VEGFA rs2010963 G>C polymorphism, the polymorphism was associated with MI risk. In conclusion, our findings suggest that VEGFA rs699947 C>A, rs3025039 C>T and rs2010963 G>C polymorphisms are risk factors for CHD. In the future, large sample size and well-designed epidemiologic studies are needed to confirm these conclusions.

11 August 2020 in Bioscience Reports
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Journal Article
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SCShuchen Chen
Shuchen Chen
RCRui Cao
Rui Cao
CLChao Liu
Chao Liu
WTWeifeng Tang
Weifeng Tang
MKMingqiang Kang
Mingqiang Kang
It is believed that an individual’s hereditary factors may be involved in the development of esophageal cancer (EC). The present study recruited 721 esophageal squamous cell carcinoma (ESCC) cases and 1208 controls and explored the roles of single nucleotide polymorphisms (SNPs) in the interleukin-4 (IL-4), IL-10, and herpesvirus entry mediator (HVEM) genes in contributing to ESCC risk. IL-4, IL-10, and HVEM SNPs were analyzed by employing an SNPscan method. After adjustment for body mass index (BMI), smoking, drinking, age and gender, we identified that the rs2070874 T>C locus in IL-4 gene decreased the risk of ESCC (CC vs. TT: P=0.008; CC vs. TT/TC: P=0.010). After a stratified analysis, we suggested that the IL-4 rs2070874 T>C variants might be a protective factor for ESCC in male, ≥63 years old, never smoking, drinking and BMI < 24 kg/m2 subgroups. In addition, we identified that the rs2243263 G>C polymorphism in IL-4 gene was a risk factor for ESCC development in the BMI ≥ 24 kg/m2 subgroup (GC vs. GG: P=0.030 and GC/CC vs. GG: P=0.018). We identified an association of the IL-4 rs2070874 T>C SNP with the decreased susceptibility of ESCC in stage I/II subgroup. Finally, we found an association of the IL-10 rs1800872 T>G SNP with a worse differentiation (TG vs. TT: P=0.048 and GG/TG vs. TT: P=0.032). In conclusion, the findings indicate a potential importance of IL-4 rs2070874 T>C, IL-4 rs2243263 G>C and IL-10 rs1800872 T>G SNPs in the development of ESCC.

17 March 2017 in Oncotarget
Verified
Journal Article
Open access
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LZLi Zhu
Li Zhu
QHQiuyu Huang
Qiuyu Huang
ZXZhiqiang Xie
Zhiqiang Xie
MKMingqiang Kang
Mingqiang Kang
HDHao Ding
Hao Ding
WTWeifeng Tang
Weifeng Tang
// <![CDATA[ $('.header-date').hide();$('#titleAuthors').hide();$('#abstractHeader').hide(); // ]]> Li Zhu1, *, Qiuyu Huang2, *, Zhiqiang Xie3, *, Mingqiang Kang4, Hao Ding5, Boyang Chen4, Yu Chen6, Chao Liu7, Yafeng Wang8 and Weifeng Tang4 1Department of Nephrology, Affiliated People’s Hospital of Jiangsu University, Zhenjiang, Jiangsu Province, China 2Department of Cardiac Surgery, Fujian Medical University Union Hospital, Fuzhou, Fujian Province, China 3Department of Clinical Laboratory, Fujian Medical University Union Hospital, Fuzhou, Fujian Province, China 4Department of Thoracic Surgery, Fujian Medical University Union Hospital, Fuzhou, Fujian Province, China 5Department of Respiratory Disease, Affiliated People’s Hospital of Jiangsu University, Zhenjiang, Jiangsu Province, China 6Department of Medical Oncology, Fujian Provincial Cancer Hospital, Fujian Medical University Cancer Hospital, Fuzhou, Fujian Province, China 7Department of Cardiothoracic Surgery, Affiliated People’s Hospital of Jiangsu University, Zhenjiang, Jiangsu Province, China 8Department of Cardiology, The People's Hospital of Xishuangbanna Dai Autonomous Prefecture, Jinghong, Yunnan Province, China *These authors have contributed equally to this work Correspondence to: Weifeng Tang, email: twf001001@126.com Yafeng Wang, email: wangyafeng0910@126.com Keywords: PPARG, PPARGC1A, PPARGC1B, polymorphism, type 2 diabetes mellitus Received: January 05, 2017 Accepted: February 13, 2017 Published: March 17, 2017 ABSTRACT It has been reported that peroxisome proliferator-activated receptor gamma (PPARG) and peroxisome proliferator-activated receptor gamma co-activator 1 (PPARGC1) family (e.g. PPARGC1A and PPARGC1B) are key agents in the development and pathophysiology of type 2 diabetes mellitus (T2DM). In this study, we designed a case-control study and selected PPARG rs1801282 C>G, PPARG rs3856806 C>T, PPARGC1A rs8192678 C>T, PPARGC1A rs2970847 C>T, PPARGC1A rs3736265 G>A, PPARGC1B rs7732671 G>C and PPARGC1B rs17572019 G>A polymorphisms to assess the relationship between these polymorphisms and T2DM using the SNPscan method. A total of 502 T2DM patients and 784 non-diabetic controls were enrolled. We found that PPARGC1A rs3736265 G>A polymorphism was correlated with a borderline decreased susceptibility of T2DM. In a subgroup analysis by age, sex, alcohol use, smoking status and body mass index, a significantly decreased risk of T2DM in G, PPARG rs3856806 C>T, PPARGC1A rs8192678 C>T, PPARGC1A rs2970847 C>T, PPARGC1A rs3736265 G>A, PPARGC1B rs7732671 G>C and PPARGC1B rs17572019 G>A polymorphisms in gene position significantly increased the risk of T2DM. However, CCCCACA haplotype conferred a decreased risk to T2DM. We also found that PPARGC1A rs3736265 A allele decreased the level of fasting plasma glucose (FPG), while increased the level of Triglyceride. In conclusion, Our findings suggest that variants of PPARGC1A rs3736265 G>A polymorphism decrease the level of FPG, improving the expectation of study in individual's prevention strategies to T2DM.

1 August 2018 in Cancer Management and Research
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SCShuchen Chen
Shuchen Chen
HQHao Qiu
Hao Qiu
CLChao Liu
Chao Liu
YWYafeng Wang
Yafeng Wang
WTWeifeng Tang
Weifeng Tang
MKMingqiang Kang
Mingqiang Kang
Background: IGF2BP2 and IGFBP3 polymorphisms may be associated with cancer risk. Methods: With an aim to determine the association of variations in IGF2BP2 and IGFBP3 genes with risk of non-small-cell lung cancer (NSCLC), IGF2BP2 rs1470579 A>C, rs4402960 G>T and IGFBP3 rs2270628 C>T, rs3110697 G>A, and rs6953668 G>A polymorphisms were selected and genotyped in 521 NSCLC patients and 1,030 controls. Results: We found that there was no difference in IGF2BP2 and IGFBP3 genotype distribution among the NSCLC patients and controls. The stratified analyses suggested that IGF2BP2 rs1470579 A>C polymorphism decreased the risk of NSCLC in some subgroups (female subgroup: CC vs AA: adjusted P=0.032 and CC vs AC/AA: adjusted P=0.028; T polymorphism decreased the risk of NSCLC in some subgroups (female subgroup: TT vs GG: adjusted P=0.031 and TT vs GT/GG: adjusted P=0.026; C, rs4402960 G>T single-nucleotide polymorphisms are candidates for decreased susceptibility to NSCLC among female, <60 years, and never drinking subgroups. In the future, more case–control studies with functional analysis are needed to confirm these preliminary findings.

18 October 2018 in Journal of Cellular Biochemistry
Verified
Journal Article
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WTWeifeng Tang
Weifeng Tang
SCShuchen Chen
Shuchen Chen
JLJun Liu
Jun Liu
CLChao Liu
Chao Liu
YWYafeng Wang
Yafeng Wang
MKMingqiang Kang
Mingqiang Kang
Esophagogastric junction adenocarcinoma (EGJA) may be associated with obesity and overweight. Thus, any variant in energy metabolism–related gene may influence the development of EGJA. In this study, we recruited 720 EGJA cases and 1541 noncancer controls. We selected IGF2BP2 rs4402960 G > T, rs1470579 A > C, IGF1 rs5742612 A > G and IGFBP3 rs3110697 G > A, rs2270628 C > T and rs6953668 G > A loci and assessed the relationship of these polymorphisms with lymph node status and susceptibility of EGJA. We found that IGF2BP2 rs1470579 A > C and IGFBP3 rs6953668 G > A polymorphisms were associated with the decreased risk of EGJA ( IGF2BP2 rs1470579: CC vs AA: adjusted odds ratio [OR] = 0.65, 95% confidence interval [CI] = 0.43‐0.98, P = 0.041 and CC vs AA/AC: adjusted OR = 0.62, 95% CI = 0.41‐0.93, P = 0.021 and IGFBP3 rs6953668: GA vs GG: adjusted OR = 0.66, 95% CI = 0.47‐0.93, P = 0.019 and GA/AA vs GG: adjusted OR = 0.68, 95% CI = 0.48‐0.95, P = 0.026). However, we also found that IGF1 rs5742612 A > G polymorphism increased the risk of LNM among patients with EGJA (GG vs AA: adjusted OR = 1.88, 95% CI = 1.02‐3.46, P = 0.042 and GG vs AA/AG: adjusted OR = 1.92, 95% CI = 1.06‐3.47, P = 0.032). This study suggests that IGF2BP2 rs1470579 A > C and IGFBP3 rs6953668 G > A polymorphisms may decrease genetic susceptibility to EGJA in eastern Chinese Han population. In addition, our findings also indicate that IGF1 rs5742612 A > G polymorphism may increase the susceptibility of LNM among patients with EGJA.

28 June 2019 in Bioscience Reports
Verified
Journal Article
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GRGuoxiang Rong
Guoxiang Rong
WTWeifeng Tang
Weifeng Tang
YWYafeng Wang
Yafeng Wang
HQHao Qiu
Hao Qiu
SCShuchen Chen
Shuchen Chen
Leptin receptor (LEPR) signaling may be involved in promoting angiogenesis and proliferation, inhibiting apoptosis and playing a vital role in the progression of carcinogenesis. A number of studies have focused on the association of LEPR rs1137101 variants with susceptibility of cancer, however, the observed results were controversial. We searched literature on the relationship of LEPR rs1137101 G>A polymorphism with cancer risk by using PubMed and Embase databases, covering all publications up to 14 October 2018. In total, 44 case–control studies with 35,936 subjects were included. After combining all eligible studies, we identified null relationship between LEPR gene rs1137101 G>A polymorphism and overall cancer risk [A vs. G: odds ratio (OR ) = 0.97, 95% confidence interval (CI ) = 0.89–1.06, P = 0.547; AA vs. GG: OR = 0.93, 95% CI = 0.78–1.13, P = 0.476; AA/GA vs. GG: OR = 0.99, 95% CI = 0.91–1.09, P= 0.890 and AA vs. GA/GG: OR = 0.92, 95% CI = 0.82–1.04, P= 0.198]. However, in a subgroup analysis, there was an increased susceptibility of oral and oropharyngeal cancer in AA vs. GA/GG genetic model (OR, 1.83; 95% CI, 1.01–3.33; P=0.048). Considering the limited participants were included, the findings might be underpowered. Sensitivity analysis identified that any independent study omitted did not materially influence the pooled ORs and CIs. The results of publication bias detection showed that there was no evidence of bias. In summary, this analysis indicates that no significant association of cancer risk was identified to be correlated with rs1137101 G>A variants, even in stratified analyses.