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33. Introduction

Author

Jiang, Hao, Chen, Qimei, Zeng, Yuanyuan, Li, Deshi, Leung, Henry, Series Editor, Jiang, Hao, Chen, Qimei, Zeng, Yuanyuan, and Li, Deshi

Published
2019
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40. N6-methyladenosine-modified SRPK1 promotes aerobic glycolysis of lung adenocarcinoma via PKM splicing.

Author

Wang, Anqi, Zeng, Yuanyuan, Zhang, Weijie, Zhao, Jian, Gao, Lirong, Li, Jianjun, Zhu, Jianjie, Liu, Zeyi, and Huang, Jian-an

Abstract

Background: The RNA N6-methyladenosine (m6A) modification has become an essential hotspot in epigenetic modulation. Serine–arginine protein kinase 1 (SRPK1) is associated with the pathogenesis of various cancers. However, the m6A modification of SRPK1 and its association with the mechanism of in lung adenocarcinoma (LUAD) remains unclear. Methods: Western blotting and polymerase chain reaction (PCR) analyses were carried out to identify gene and protein expression. m6A epitranscriptomic microarray was utilized to the assess m6A profile. Loss and gain-of-function assays were carried out elucidate the impact of METTL3 and SRPK1 on LUAD glycolysis and tumorigenesis. RNA immunoprecipitation (RIP), m6A RNA immunoprecipitation (MeRIP), and RNA stability tests were employed to elucidate the SRPK1's METTL3-mediated m6A modification mechanism in LUAD. Metabolic quantification and co-immunoprecipitation assays were applied to investigate the molecular mechanism by which SRPK1 mediates LUAD metabolism. Results: The epitranscriptomic microarray assay revealed that SRPK1 could be hypermethylated and upregulated in LUAD. The main transmethylase METTL3 was upregulated and induced the aberrant high m6A levels of SRPK1. Mechanistically, SRPK1's m6A sites were directly methylated by METTL3, which also stabilized SRPK1 in an IGF2BP2-dependent manner. Methylated SRPK1 subsequently promoted LUAD progression through enhancing glycolysis. Further metabolic quantification, co-immunoprecipitation and western blot assays revealed that SRPK1 interacts with hnRNPA1, an important modulator of PKM splicing, and thus facilitates glycolysis by upregulating PKM2 in LUAD. Nevertheless, METTL3 inhibitor STM2457 can reverse the above effects in vitro and in vivo by suppressing SRPK1 and glycolysis in LUAD. Conclusion: It was revealed that in LUAD, aberrantly expressed METTL3 upregulated SRPK1 levels via an m6A-IGF2BP2-dependent mechanism. METTL3-induced SRPK1 fostered LUAD cell proliferation by enhancing glycolysis, and the small-molecule inhibitor STM2457 of METTL3 could be an alternative novel therapeutic strategy for individuals with LUAD. [ABSTRACT FROM AUTHOR]

Published
2024
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41. Association of education attainment and risk of connective tissue diseases.

Author

Zeng, Yuanyuan, Yang, Xiaolan, Tao, Shengda, and Lei, Ling

Subjects
*CONNECTIVE tissue diseases, *SYSTEMIC lupus erythematosus, *GENOME-wide association studies, *SYSTEMIC scleroderma, *DERMATOMYOSITIS
Abstract

Objective: We employed two‐sample Mendelian randomization (MR) to assess the genetic causal relationship between educational attainment (EA) and risk of five common connective tissue diseases (CTDs). Methods: Educational attainment (self‐reported at age ≥30 years) was obtained from a meta‐analysis of years of schooling in 766 345 participants of European ancestry from genome‐wide association studies (GWAS). A total of 1265 signals associated with EA were identified. Genetic data for five CTDs [rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), systemic sclerosis (SSc), polymyositis (PM), and dermatomyositis (DM)] were obtained from the FinnGen consortium. Two‐sample MR analyses were performed separately for EA and the five CTDs. Results: We found a negative causal relationship between EA and RA (ORIVW = 0.627, 95% CI = 0.537–0.732, p <.001), and SLE (ORIVW = 0.341, 95% CI = 0.123–0.944, p =.038). There were no genetic causal association between EA and SSc (ORIVW = 0.647, 95% CI = 0.351–1.195, p =.164), PM (ORIVW = 0.938, 95% CI = 0.320–2.746, p =.907), or DM (ORIVW = 0.754, 95% CI = 0.351–1.619, p =.468). None of the analyses revealed any horizontal pleiotropy or heterogeneity. Conclusion: Our findings indicated a potential causal association between EA and RA, SLE, emphasizing the need for further investigation and potential integration of EA into clinical practice to enhance treatment strategies. [ABSTRACT FROM AUTHOR]

Published
2024
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42. Distributed Multiple-Service User-Experience Energy Saving Algorithm for Base Station

Author

Zeng, Yuanyuan, Zhang, Yu, Jiang, Hao, Zhou, Xian, Akan, Ozgur, Editorial Board Member, Bellavista, Paolo, Editorial Board Member, Cao, Jiannong, Editorial Board Member, Coulson, Geoffrey, Editorial Board Member, Dressler, Falko, Editorial Board Member, Ferrari, Domenico, Editorial Board Member, Gerla, Mario, Editorial Board Member, Kobayashi, Hisashi, Editorial Board Member, Palazzo, Sergio, Editorial Board Member, Sahni, Sartaj, Editorial Board Member, Shen, Xuemin (Sherman), Editorial Board Member, Stan, Mircea, Editorial Board Member, Xiaohua, Jia, Editorial Board Member, Zomaya, Albert Y., Editorial Board Member, Leung, Victor C. M., editor, Zhang, Haijun, editor, Hu, Xiping, editor, Liu, Qiang, editor, and Liu, Zhi, editor

Published
2019
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43. A Space Dynamic Discovery Scheme for Crowd Flow of Urban City

Author

Wang, Zhaojun, Jiang, Hao, Zhao, Xiaoyue, Zeng, Yuanyuan, Zhang, Yi, Du, Wen, Goos, Gerhard, Founding Editor, Hartmanis, Juris, Founding Editor, Bertino, Elisa, Editorial Board Member, Gao, Wen, Editorial Board Member, Steffen, Bernhard, Editorial Board Member, Woeginger, Gerhard, Editorial Board Member, Yung, Moti, Editorial Board Member, and Qiu, Meikang, editor

Published
2019
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44. Smart Custom Package Decision for Mobile Internet Services

Author

Yang, Zhian, Zheng, Cong, Jiang, Hao, Zeng, Yuanyuan, Hu, Zhiyi, Du, Wen, Goos, Gerhard, Founding Editor, Hartmanis, Juris, Founding Editor, Bertino, Elisa, Editorial Board Member, Gao, Wen, Editorial Board Member, Steffen, Bernhard, Editorial Board Member, Woeginger, Gerhard, Editorial Board Member, Yung, Moti, Editorial Board Member, and Qiu, Meikang, editor

Published
2019
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45. Do Top Social Apps Effect Voice Call? Evidence from Propensity Score Matching Methods

Author

Jiang, Hao, Lin, Min, Liu, Bingqing, Liu, Huifang, Zeng, Yuanyuan, Nai, He, Zhang, Xiaoli, Zhao, Xianlong, Du, Wen, Ye, Haining, Goos, Gerhard, Founding Editor, Hartmanis, Juris, Founding Editor, Bertino, Elisa, Editorial Board Member, Gao, Wen, Editorial Board Member, Steffen, Bernhard, Editorial Board Member, Woeginger, Gerhard, Editorial Board Member, Yung, Moti, Editorial Board Member, and Qiu, Meikang, editor

Published
2019
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