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Your search keyword '"Zou, Sailan"' showing total 17 results
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17 results on '"Zou, Sailan"'

3. A microRNA checkpoint for Ca2+ signaling and overload in acute pancreatitis

Author

Du, Wenya, Liu, Geng, Shi, Na, Tang, Dongmei, Ferdek, Pawel E., Jakubowska, Monika A., Liu, Shiyu, Zhu, Xinyue, Zhang, Jiayu, Yao, Linbo, Sang, Xiongbo, Zou, Sailan, Liu, Tingting, Mukherjee, Rajarshi, Criddle, David N., Zheng, Xiaofeng, Xia, Qing, Berggren, Per-Olof, Huang, Wendong, Sutton, Robert, Tian, Yan, Huang, Wei, and Fu, Xianghui

Published
2022
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5. On Energy Optimization for Hierarchical Federated Learning With Delay Constraint Through Node Cooperation

Author

Li, Zhuo, Zou, Sailan, Guo, Song, Li, Zhuo, Zou, Sailan, and Guo, Song

Abstract

In hierarchical federated learning (HFL), edge computing is introduced for partial model aggregation to reduce latency. High energy cost is an important issue to be solved in the process of parameters uploading. Our study focuses on the issue of minimizing energy cost with delay constraint through node cooperation in HFL, and the decision problem for this is NP-hard. We introduce a cost-efficient HFL (CE-HFL) framework, where nodes not only participate in model training but also transmit and aggregate model parameters for neighbors. A parameter aggregation tree is first generated, and parameter updates can be delivered to edge servers along paths in the tree while being aggregated simultaneously. Through theoretical analysis, it is proved that CE-HFL can achieve energy optimization with delay constraint. We also evaluate its performance through thorough experiments. In comparison with HierFAVG, CFL, and HFEL, it is found that CE-HFL can save energy cost up to 24.58%, 22.02%, and 6.60%, respectively. © 2014 IEEE.

Published
2024

10. Extrachromosomal circular MiR-17-92 amplicon promotes HCC

Author

Zou, Sailan, primary, Chen, Shihan, additional, Rao, Guocheng, additional, Zhang, Guixiang, additional, Ma, Meilin, additional, Peng, Boqiang, additional, Du, Xiao, additional, Huang, Wei, additional, Lin, Weiqiang, additional, Tian, Yan, additional, and Fu, Xianghui, additional

Published
2023
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12. Targeting RNA G-quadruplex with repurposed drugs blocks SARS-CoV-2 entry

Author

Tong, Qiyu, primary, Liu, Geng, additional, Sang, Xiongbo, additional, Zhu, Xinyue, additional, Fu, Xiaoli, additional, Dou, Chao, additional, Jian, Yue, additional, Zhang, Jiani, additional, Zou, Sailan, additional, Zhang, Guixiang, additional, Du, Xiao, additional, Liu, Dan, additional, Qi, Shiqian, additional, Cheng, Wei, additional, Tian, Yan, additional, and Fu, Xianghui, additional

Published
2023
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13. Circular RNA circDVL1 inhibits clear cell renal cell carcinoma progression through the miR-412-3p/PCDH7 axis

Author

Wang, Ying, primary, Zhang, Yunjing, additional, Su, Xinwan, additional, Qiu, Qiongzi, additional, Yuan, Yuan, additional, Weng, Chunhua, additional, Zou, Sailan, additional, Tian, Yan, additional, Han, Weidong, additional, Liu, Pengyuan, additional, Guo, Xingyi, additional, Mao, Jianhua, additional, Fu, Xianghui, additional, Wang, Ping, additional, and Lin, Weiqiang, additional

Published
2022
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14. An Endoplasmic Reticulum Stress–Micro RNA ‐26a Feedback Circuit in NAFLD

Author

Xu, Haixia, primary, Tian, Yan, additional, Tang, Dongmei, additional, Zou, Sailan, additional, Liu, Geng, additional, Song, Jiulin, additional, Zhang, Guixiang, additional, Du, Xiao, additional, Huang, Wei, additional, He, Bin, additional, Lin, Weiqiang, additional, Jin, Liang, additional, Huang, Wendong, additional, Yang, Jiayin, additional, and Fu, Xianghui, additional

Published
2020
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16. A microRNA checkpoint for Ca2+signaling and overload in acute pancreatitis

Author

Du, Wenya, Liu, Geng, Shi, Na, Tang, Dongmei, Ferdek, Pawel E., Jakubowska, Monika A., Liu, Shiyu, Zhu, Xinyue, Zhang, Jiayu, Yao, Linbo, Sang, Xiongbo, Zou, Sailan, Liu, Tingting, Mukherjee, Rajarshi, Criddle, David N., Zheng, Xiaofeng, Xia, Qing, Berggren, Per-Olof, Huang, Wendong, Sutton, Robert, Tian, Yan, Huang, Wei, and Fu, Xianghui

Abstract

Acute pancreatitis (AP) is a common digestive disease without specific treatment, and its pathogenesis features multiple deleterious amplification loops dependent on translation, triggered by cytosolic Ca2+([Ca2+]i) overload; however, the underlying mechanisms in Ca2+overload of AP remains incompletely understood. Here we show that microRNA-26a (miR-26a) inhibits pancreatic acinar cell (PAC) store-operated Ca2+entry (SOCE) channel expression, Ca2+overload, and AP. We find that major SOCE channels are post-transcriptionally induced in PACs during AP, whereas miR-26a expression is reduced in experimental and human AP and correlated with AP severity. Mechanistically, miR-26a simultaneously targets Trpc3and Trpc6SOCE channels and attenuates physiological oscillations and pathological elevations of [Ca2+]iin PACs. MiR-26a deficiency increases SOCE channel expression and [Ca2+]ioverload, and significantly exacerbates AP. Conversely, global or PAC-specific overexpression of miR-26a in mice ameliorates pancreatic edema, neutrophil infiltration, acinar necrosis, and systemic inflammation, accompanied with remarkable improvements on pathological determinants related with [Ca2+]ioverload. Moreover, pancreatic or systemic administration of an miR-26a mimic to mice significantly alleviates experimental AP. These findings reveal a previously unknown mechanism underlying AP pathogenesis, establish a critical role for miR-26a in Ca2+signaling in the exocrine pancreas, and identify a potential target for the treatment of AP.

Published
2022
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17. Extrachromosomal circular MiR-17-92 amplicon promotes HCC.

Author

Zou S, Chen S, Rao G, Zhang G, Ma M, Peng B, Du X, Huang W, Lin W, Tian Y, and Fu X

Subjects
Humans, DNA, Circular genetics, Polymerase Chain Reaction, Carcinoma, Hepatocellular genetics, Liver Neoplasms genetics, MicroRNAs genetics, Multigene Family
Abstract

Background and Aims: Extrachromosomal circular DNAs (eccDNAs) are prevalent in cancer genomes and emerge as a class of crucial yet less characterized oncogenic drivers. However, the structure, composition, genome-wide frequency, and contribution of eccDNAs in HCC, one of the most fatal and prevalent cancers, remain unexplored. In this study, we provide a comprehensive characterization of eccDNAs in human HCC and demonstrate an oncogenic role of microRNA (miRNA)-17-92-containing eccDNAs in tumor progression., Approach and Results: Using the circle-sequencing method, we identify and characterize more than 230,000 eccDNAs from 4 paired samples of HCC tumor and adjacent nontumor liver tissues. EccDNAs are highly enriched in HCC tumors, preferentially originate from certain chromosomal hotspots, and are correlated with differential gene expression. Particularly, a series of eccDNAs carrying the miRNA-17-92 cluster are validated by outward PCR and Sanger sequencing. Quantitative PCR analyses reveal that miRNA-17-92-containing eccDNAs, along with the expression of their corresponding miRNAs, are elevated in HCC tumors and associated with poor outcomes and the age of HCC patients. More intriguingly, exogenous expression of artificial DNA circles harboring the miR-17-92 cluster, which is synthesized by the ligase-assisted minicircle accumulation method, can significantly accelerate HCC cell proliferation and migration., Conclusions: These findings delineate the genome-wide eccDNAs profiling of HCC and highlight the functional significance of miRNA-containing eccDNAs in tumorigenesis, providing insight into HCC pathogenesis and cancer therapy, as well as eccDNA and miRNA biology., (Copyright © 2023 American Association for the Study of Liver Diseases.)

Published
2024
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