6 results on '"Yuya Wang"'
Search Results
2. Different polymorphisms in HIF-1α may exhibit different effects on cancer risk in Asians: evidence from nearly forty thousand participants
- Author
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Minjie Chu, Xiaoyi Zhou, Xiaoqi Zhu, Yuya Wang, Yueping Zhong, Jingsheng Xu, Jingwen Cheng, Liu Yichen, and Xiaoyu Fu
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Oncology ,Male ,Aging ,medicine.medical_specialty ,Asia ,HIF-1α ,Single-nucleotide polymorphism ,survival ,Polymorphism, Single Nucleotide ,Risk Assessment ,polymorphism ,Asian People ,Risk Factors ,Pancreatic cancer ,Internal medicine ,Neoplasms ,Genotype ,expression ,Medicine ,cancer ,Humans ,Genetic Predisposition to Disease ,Allele ,Lung cancer ,Survival analysis ,Genetic Association Studies ,business.industry ,Cell Biology ,medicine.disease ,Hypoxia-Inducible Factor 1, alpha Subunit ,Head and neck squamous-cell carcinoma ,Phenotype ,Case-Control Studies ,Disease Progression ,Female ,business ,Cancer risk ,Research Paper - Abstract
The effect of different SNPs in HIF-1α and cancer susceptibility remain indistinct. Here, we evaluated the association between all identified SNPs (rs11549465, rs11549467 and rs2057482) in HIF-1α and the overall risk of cancer in all case-control studies published before April 2020. A total of 54 articles including 56 case-control studies were included in this analysis. We found that variant genotypes of rs11549465 and rs11549467 were associated with a significantly increased overall cancer risk. In contrast, the variant T allele of rs2057482 showed a significantly reduced risk of overall cancer. In addition, variant genotypes of the three studied SNPs exhibited a significant association with cancer risk in Asians and specific cancer types. Meanwhile, HIF-1α was significantly highly expressed in head and neck squamous cell carcinoma and pancreatic cancer tissues. More importantly, survival analysis indicated that the high expression of HIF-1α was associated with a poor survival in patients with lung cancer. These findings further provided evidence that different SNPs in HIF-1α may exhibit different effects on overall cancer risk; these effects were ethnicity and type-specific. Further studies with functional evaluations are required to confirm the biological mechanisms underlying the role of HIF-1α SNPs in cancer development and progression.
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- 2020
3. RNA 5-Methylcytosine Regulators Contribute to Metabolism Heterogeneity and Predict Prognosis in Ovarian Cancer
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Jie Xu, Xiaoyi Liu, Yanjie Chen, Yuya Wang, Tao Liu, and Ping Yi
- Subjects
Cell Biology ,Developmental Biology - Abstract
5-Methylcytosine (m5C) is an abundant and highly conserved modification in RNAs. The dysregulation of RNA m5C methylation has been reported in cancers, but the regulatory network in ovarian cancer of RNA m5C methylation-related genes and its implication in metabolic regulation remain largely unexplored. In this study, RNA-sequencing data and clinical information of 374 ovarian cancer patients were downloaded from The Cancer Genome Atlas database, and a total of 14 RNA m5C regulators were included. Through unsupervised consensus clustering, two clusters with different m5C modification patterns were identified with distinct survivals. According to enrichment analyses, glycosaminoglycan and collagen metabolism–related pathways were specifically activated in cluster 1, whereas fatty acid metabolism–related pathways were enriched in cluster 2, which had better overall survival (OS). Besides the metabolism heterogeneity, the higher sensitivity to platinum and paclitaxel in cluster 2 can further explain the improved OS. Ultimately, a least absolute shrinkage and selection operator prediction model formed by ALYREF, NOP2, and TET2 toward OS was constructed. In conclusion, distinct m5C modification pattern exhibited metabolism heterogeneity, different chemotherapy sensitivity, and consequently survival difference, providing evidence for risk stratification.
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- 2021
4. Substituted 3-benzylcoumarins 13 and 14 suppress enterovirus A71 replication by impairing viral 2Apro dependent IRES-driven translation
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Yan Niu, Chao Wang, Hao Zhang, Xin Wang, Yihong Peng, Ping Xu, Yuya Wang, and Xinyi Pei
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0301 basic medicine ,Pharmacology ,MAPK/ERK pathway ,Sorafenib ,Chemistry ,Kinase ,MEK inhibitor ,030106 microbiology ,Cell biology ,03 medical and health sciences ,Internal ribosome entry site ,030104 developmental biology ,Viral replication ,Mechanism of action ,Virology ,medicine ,medicine.symptom ,Cytotoxicity ,medicine.drug - Abstract
Activation of the ERK signaling cascade in host cells has been demonstrated to be essential for enterovirus A71 (EV-A71) replication. Our previous study showed that MEK kinase, which specially activated downstream ERK kinase, is an important and potential target against EV-A71. Furthermore, we reported that a series of substituted 3-benzylcoumarins designed and synthesized as well as verified for inhibiting the MEK-ERK cascade were found to be effective on anti-EV-A71. In this study, we further demonstrated that two substituted 3-benzylcoumarins designated as 13 and 14 were more effective anti-MEK/ERK activity, less cytotoxicity and stronger antiviral effect represented by inhibition of viral-induced CPE, the expression of viral proteins and the replication of the viral genome, as well as the production of progeny virions, compared to those of U0126, an available MEK inhibitor, and sorafenib, a multiple-targeted kinase inhibitor in clinical use. Moreover, we explored that the likely mechanism of action of these two test compounds were to block EV-A71 2A dependent IRES-driven activity essential for successful viral replication. Hence, our results suggest that two substituted 3-benzylcoumarins 13 and 14 could be candidates as potential anti-EV-A71 agents.
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- 2018
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5. Regulation of enterovirus 2A protease-associated viral IRES activities by the cell's ERK signaling cascade: Implicating ERK as an efficiently antiviral target
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Chao Xu, Meng Zhu, Jing Sun, Ping Xu, Yihong Peng, Hao Zhang, Hao Duan, Yuya Wang, Qing Xiong, and Chao Wang
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0301 basic medicine ,MAPK/ERK pathway ,Small interfering RNA ,viruses ,medicine.medical_treatment ,030106 microbiology ,Cell ,Internal Ribosome Entry Sites ,Biology ,Virus Replication ,Antiviral Agents ,Viral Proteins ,03 medical and health sciences ,chemistry.chemical_compound ,Cell Line, Tumor ,Virology ,Nitriles ,Rhabdomyosarcoma ,Butadienes ,Enterovirus Infections ,medicine ,Humans ,RNA, Small Interfering ,Polyproteins ,Pharmacology ,Protease ,EIF4G ,Viral translation ,Enterovirus A, Human ,Cell biology ,Enzyme Activation ,Internal ribosome entry site ,HEK293 Cells ,030104 developmental biology ,medicine.anatomical_structure ,Viral replication ,chemistry ,Mutagenesis, Site-Directed ,Signal Transduction - Abstract
In a previous study the ERK1/2 pathway was found to be crucially involved in positive regulation of the enterovirus A 71(EV-A71) IRES (vIRES), thereby contributing to the efficient replication of an important human enterovirus causing death in young children (
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- 2017
- Full Text
- View/download PDF
6. Med23 serves as a gatekeeper of the myeloid potential of hematopoietic stem cells
- Author
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Yuling Dai, Yuya Wang, Fan Guo, Xiaoyan Zhu, Xufeng Chen, Pei Hao, Hao Shen, Yu Cui, Yuanhua Liu, Guangrong Song, Jingyao Zhao, Haifeng Liu, Xiaolong Liu, Chan Gu, and Huayue Xing
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0301 basic medicine ,Myeloid ,Science ,General Physics and Astronomy ,Biology ,General Biochemistry, Genetics and Molecular Biology ,03 medical and health sciences ,Gene Knockout Techniques ,Mice ,Transcription (biology) ,Stress, Physiological ,medicine ,Animals ,Myeloid Cells ,Progenitor cell ,Cell Self Renewal ,lcsh:Science ,Gene ,Myeloid Progenitor Cells ,Bone Marrow Transplantation ,Regulation of gene expression ,Multidisciplinary ,Mediator Complex ,hemic and immune systems ,Cell Differentiation ,General Chemistry ,medicine.disease ,Hematopoietic Stem Cells ,Cell biology ,Hematopoiesis ,Haematopoiesis ,030104 developmental biology ,medicine.anatomical_structure ,Gene Expression Regulation ,lcsh:Q ,Lymphocytopenia ,Stem cell - Abstract
In response to myeloablative stresses, HSCs are rapidly activated to replenish myeloid progenitors, while maintaining full potential of self-renewal to ensure life-long hematopoiesis. However, the key factors that orchestrate HSC activities during physiological stresses remain largely unknown. Here we report that Med23 controls the myeloid potential of activated HSCs. Ablation of Med23 in hematopoietic system leads to lymphocytopenia. Med23-deficient HSCs undergo myeloid-biased differentiation and lose the self-renewal capacity. Interestingly, Med23-deficient HSCs are much easier to be activated in response to physiological stresses. Mechanistically, Med23 plays essential roles in maintaining stemness genes expression and suppressing myeloid lineage genes expression. Med23 is downregulated in HSCs and Med23 deletion results in better survival under myeloablative stress. Altogether, our findings identify Med23 as a gatekeeper of myeloid potential of HSCs, thus providing unique insights into the relationship among Med23-mediated transcriptional regulations, the myeloid potential of HSCs and HSC activation upon stresses.
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- 2017
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