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33 results on '"Zhang, Erbao"'

8. Multi-omics analysis reveals NNMT as a master metabolic regulator of metastasis in esophageal squamous cell carcinoma

Author

Huang, Qi, primary, Chen, Haiming, additional, Yin, Dandan, additional, Wang, Jie, additional, Wang, Shaodong, additional, Yang, Feng, additional, Li, Jiawei, additional, Mu, Teng, additional, Li, Jilun, additional, Zhao, Jia, additional, Yin, Rong, additional, Li, Wei, additional, Qiu, Mantang, additional, Zhang, Erbao, additional, and Li, Xiangnan, additional

Published
2024
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9. Integrative analyses of N6‐methyladenosine‐associated single‐nucleotide polymorphisms (m6A‐SNPs) identify tumor suppressor gene AK9 in lung cancer

Author

Hua, Tingting, primary, Zhang, Chang, additional, Fu, Yating, additional, Qin, Na, additional, Liu, Su, additional, Chen, Congcong, additional, Gong, Linnan, additional, Ma, Huimin, additional, Ding, Yue, additional, Wei, Xiaoxia, additional, Jin, Chenying, additional, Jin, Chen, additional, Zhu, Meng, additional, Zhang, Erbao, additional, Dai, Juncheng, additional, and Ma, Hongxia, additional

Published
2023
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10. Long noncoding RNA NRAV in the 12q24.31 risk locus drives gastric cancer development through glucose metabolism reprogramming

Author

Zhang, Yan, primary, Gao, Yun, additional, Li, Fengyuan, additional, Qi, Qi, additional, Li, Qian, additional, Gu, Yuanliang, additional, Zheng, Zhonghua, additional, Hu, Beiping, additional, Wang, Tianpei, additional, Zhang, Erbao, additional, Xu, Hao, additional, Liu, Li, additional, Tian, Tian, additional, Jin, Guangfu, additional, and Yan, Caiwang, additional

Published
2023
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12. Long non-coding RNA NRAV in the 12q24.31 risk locus drives gastric cancer development through glucose metabolism reprogramming.

Author

Zhang, Yan, Gao, Yun, Li, Fengyuan, Qi, Qi, Li, Qian, Gu, Yuanliang, Zheng, Zhonghua, Hu, Beiping, Wang, Tianpei, Zhang, Erbao, Xu, Hao, Liu, Li, Tian, Tian, Jin, Guangfu, and Yan, Caiwang

Abstract

Long non-coding RNAs (lncRNAs) serve as vital candidates to mediate cancer risk. Here, we aimed to identify the risk single-nucleotide polymorphisms (SNPs)-induced lncRNAs and to investigate their roles in gastric cancer (GC) development. Through integrating the differential expression analysis of lncRNAs in GC tissues and expression quantitative trait loci analysis in normal stomach tissues and GC tissues, as well as genetic association analysis based on GC genome-wide association studies and an independent validation study, we identified four lncRNA-related SNPs consistently associated with GC risk, including SNHG7 [odds ratio (OR) = 1.16, 95% confidence interval (CI): 1.09–1.23], NRAV (OR = 1.11, 95% CI: 1.05–1.17), LINC01082 (OR = 1.16, 95% CI: 1.08–1.22) and FENDRR (OR = 1.16, 95% CI: 1.07–1.25). We further found that a functional SNP rs6489786 at 12q24.31 increases binding of MEOX1 or MEOX2 at a distal enhancer and results in up-regulation of NRAV. The functional assays revealed that NRAV accelerates GC cell proliferation while inhibits GC cell apoptosis. Mechanistically, NRAV decreases the expression of key subunit genes through the electron transport chain, thereby driving the glucose metabolism reprogramming from aerobic respiration to glycolysis. These findings suggest that regulating lncRNA expression is a crucial mechanism for risk-associated variants in promoting GC development. [ABSTRACT FROM AUTHOR]

Published
2024
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13. METTL3‐stabilized super enhancers‐lncRNA SUCLG2‐AS1 mediates the formation of a long‐range chromatin loop between enhancers and promoters of SOX2 in metastasis and radiosensitivity of nasopharyngeal carcinoma

Author

Hu, Xinyu, primary, Wu, Jianfeng, additional, Feng, Yong, additional, Ma, Hongxia, additional, Zhang, Erbao, additional, Zhang, Chang, additional, Sun, Qi, additional, Wang, Tingting, additional, Ge, Yizhi, additional, Zong, Dan, additional, Chen, Wei, additional, and He, Xia, additional

Published
2023
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24. Additional file 1 of B4GALT1 promotes immune escape by regulating the expression of PD-L1 at multiple levels in lung adenocarcinoma

Author

Cui, Yanan, Li, Jun, Zhang, Pengpeng, Yin, Dandan, Wang, Ziyu, Dai, Jiali, Wang, Wei, Zhang, Erbao, and Guo, Renhua

Abstract

Additional file 1: Figure S1. (A-B) qRT-PCR was performed to detect the B4GALT1 mRNA expression after siRNA-mediated knockdown and plasmid-mediated overexpression in A549 and PC9 cells. (C) Western blot was performed to detect the B4GALT1 protein expression. (D) The protein expression levels of CDK4 and Cyclin D1 in control and ectopic B4GALT1-expressing A549 and PC9 cells were determined using western blotting analyses. * P < 0.05, ** P < 0.01. Figure S2. (A) The linear correlations between the B4GALT1 expression and the CD8+ T-cell expression in the TCGA-LUAD dataset. (B) Comparison of TIDE scores between the B4GALT1-high group and B4GALT1-low group. (C) Comparison of overall survival between CTL top (samples above average CTL values among all samples) and CTL bottom (samples below average CTL values among all samples) groups in patients with different B4GALT1 levels. The two-sided Wald test in the Cox-PH regression was applied to compute the association between the CTL level and overall survival, and samples were split by the best separation strategy according to the B4GALT1 expression coefficients in the Cox-PH regression model. ** P < 0.01. Figure S3. (A-B) The differential expression of CD274 in tumours with high expression of B4GALT1 and low expression of B4GALT1 in the CCLE mRNA dataset (A) and the differential expression of PD-L1 in tumours with high expression of B4GALT1 and low expression of B4GALT1 in the TCGA-protein dataset (B). RPKM: reads per kilobase per million mapped reads; RPPA: reverse phase protein array. (C) Representative immunohistochemical images (left panel) and the association between B4GALT1 and PD-L1 level in MPLC tumours (right panel). Scale bars, 200 μm. (D) qRT-PCR was performed to detect the B4galt1 mRNA expression after siRNA-mediated knockdown in LLC cells. (E-F) LLC cells were transfected with si-B4galt1 or pcDNA- B4galt1, and Cd274 mRNA and PD-L1 protein was analysed by qRT-PCR and western blotting analyses. (G) LLC cells cocultured with activated CD8+ T cells for 48 h were subjected to crystal violet staining and quantified at 570 nm. The ratio of LLC cells to T cells is 1:3. (H) Western blot analysis of PD-L1 expression in LLC cells with or without the knockdown or overexpression of B4galt1 followed by the treatment with CHX. (I) Western blot analysis of PD-L1 levels in B4galt1 knock-down cells, B4galt1 overexpression cells, and tunicamycin (TM) treated cells. * P < 0.05, ** P < 0.01, ****P

Published
2023
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27. Gene amplification‐driven RNA methyltransferase KIAA1429 promotes tumorigenesis by regulating BTG2 via m6A‐YTHDF2‐dependent in lung adenocarcinoma

Author

Zhang, Chang, primary, Sun, Qi, additional, Zhang, Xu, additional, Qin, Na, additional, Pu, Zhening, additional, Gu, Yayun, additional, Yan, Caiwang, additional, Zhu, Meng, additional, Dai, Juncheng, additional, Wang, Cheng, additional, Li, Ni, additional, Jin, Guangfu, additional, Ma, Hongxia, additional, Hu, Zhibin, additional, Zhang, Erbao, additional, Tan, Fengwei, additional, and Shen, Hongbing, additional

Published
2022
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28. Additional file 2 of Cancer-associated fibroblast-specific lncRNA LINC01614 enhances glutamine uptake in lung adenocarcinoma

Author

Liu, Tongyan, Han, Chencheng, Fang, Panqi, Ma, Zhifei, Wang, Xiaoxiao, Chen, Hao, Wang, Siwei, Meng, Fanchen, Wang, Cheng, Zhang, Erbao, Dong, Guozhang, Zhu, Hongyu, Yin, Wenda, Wang, Jie, Zuo, Xianglin, Qiu, Mantang, Wang, Jinke, Qian, Xu, Shen, Hongbing, Xu, Lin, Hu, Zhibin, and Yin, Rong

Abstract

Additional file 2. Supplementary Figures.

Published
2022
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32. Genetic variants associated with expression of TCF19contribute to the risk of head and neck cancer in Chinese population

Author

Ji, Pei, Chang, Jiang, Wei, Xiaoyu, Song, Xueyao, Yuan, Hua, Gong, Linnan, Li, Yuancheng, Ding, Dongsheng, Zhang, Erbao, Yan, Caiwang, Zhu, Meng, Miao, Xiaoping, Wu, Chen, Jin, Guangfu, Hu, Zhibin, Shen, Hongbing, and Ma, Hongxia

Abstract

BackgroundSquamous cell carcinoma of the head and neck (SCCHN) is one of the most common cancers worldwide and includes cancers arising from the oral cavity, pharynx and larynx. Genome-wide association studies have found several genetic variants related to the risk of SCCHN; however, they could only explain a small fraction of the heritability. Thus, more susceptibility loci associated with SCCHN need to be identified.MethodsAn association study was conducted by genotyping 555 patients with SCCHN and 1367 controls in a Chinese population. Single-variant association analysis was conducted on 63 373 SNPs, and the promising variants were then confirmed by a two-stage validation with 1875 SCCHN cases and 4637 controls. Bioinformatics analysis and functional assays were applied to uncover the potential pathogenic mechanism of the promising variants and genes associated with SCCHN.ResultsWe first identified three novel genetic variants significantly associated with the risk of SCCHN (p=7.45×10−7for rs2517611 at 6p22.1, p=1.76×10−9for rs2524182 at 6p21.33 and p=2.17×10−10for rs3131018 at 6p21.33). Further analysis and biochemical assays showed that rs3094187, which was in a region in high linkage disequilibrium with rs3131018, could modify TCF19expression by regulating the binding affinity of the transcription factor SREBF1to the promoter of TCF19. In addition, experiments revealed that the inhibition of TCF19may affect several important pathways involved in tumourigenesis and attenuate the cell proliferation and migration of SCCHN.ConclusionThese findings offer important evidence that functional genetic variants could contribute to development of SCCHN and that TCF19may function as a putative susceptibility gene for SCCHN.

Published
2022
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33. Genetic variants associated with expression of TCF19 contribute to the risk of head and neck cancer in Chinese population.

Author

Ji P, Chang J, Wei X, Song X, Yuan H, Gong L, Li Y, Ding D, Zhang E, Yan C, Zhu M, Miao X, Wu C, Jin G, Hu Z, Shen H, and Ma H

Subjects
Case-Control Studies, China epidemiology, Genetic Predisposition to Disease, Genome-Wide Association Study, Genotype, Humans, Polymorphism, Single Nucleotide genetics, Squamous Cell Carcinoma of Head and Neck genetics, Transcription Factors genetics, Carcinoma, Squamous Cell epidemiology, Carcinoma, Squamous Cell genetics, Carcinoma, Squamous Cell metabolism, Head and Neck Neoplasms epidemiology, Head and Neck Neoplasms genetics
Abstract

Background: Squamous cell carcinoma of the head and neck (SCCHN) is one of the most common cancers worldwide and includes cancers arising from the oral cavity, pharynx and larynx. Genome-wide association studies have found several genetic variants related to the risk of SCCHN; however, they could only explain a small fraction of the heritability. Thus, more susceptibility loci associated with SCCHN need to be identified., Methods: An association study was conducted by genotyping 555 patients with SCCHN and 1367 controls in a Chinese population. Single-variant association analysis was conducted on 63 373 SNPs, and the promising variants were then confirmed by a two-stage validation with 1875 SCCHN cases and 4637 controls. Bioinformatics analysis and functional assays were applied to uncover the potential pathogenic mechanism of the promising variants and genes associated with SCCHN., Results: We first identified three novel genetic variants significantly associated with the risk of SCCHN (p=7.45×10 -7 for rs2517611 at 6p22.1, p=1.76×10 -9 for rs2524182 at 6p21.33 and p=2.17×10 -10 for rs3131018 at 6p21.33). Further analysis and biochemical assays showed that rs3094187, which was in a region in high linkage disequilibrium with rs3131018, could modify TCF19 expression by regulating the binding affinity of the transcription factor SREBF1 to the promoter of TCF19 . In addition, experiments revealed that the inhibition of TCF19 may affect several important pathways involved in tumourigenesis and attenuate the cell proliferation and migration of SCCHN., Conclusion: These findings offer important evidence that functional genetic variants could contribute to development of SCCHN and that TCF19 may function as a putative susceptibility gene for SCCHN., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2022. No commercial re-use. See rights and permissions. Published by BMJ.)

Published
2022
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