Search

Your search keyword '"Sun, Linxiao"' showing total 48 results
Start Over Author "Sun, Linxiao" Publication Year Range Last 10 years
48 results on '"Sun, Linxiao"'

2. How to Improve the Teaching Effectiveness of the Second Classroom of Primary School Information Technology From the Perspective of 'Double Reduction'

Author

Wang, Weijuan, Zou, Chunjie, Dong, Zhuoyue, Sun, Qigong, Yin, Dongxin, Sun, Linxiao, Striełkowski, Wadim, Editor-in-Chief, Black, Jessica M., Series Editor, Butterfield, Stephen A., Series Editor, Chang, Chi-Cheng, Series Editor, Cheng, Jiuqing, Series Editor, Dumanig, Francisco Perlas, Series Editor, Al-Mabuk, Radhi, Series Editor, Scheper-Hughes, Nancy, Series Editor, Urban, Mathias, Series Editor, Webb, Stephen, Series Editor, Khan, Intakhab Alam, editor, Yu, Zhonggen, editor, Birkök, Mehmet Cüneyt, editor, and Abu Bakar, Abu Yazid, editor

Published
2024
Full Text
View/download PDF

27. Baohuoside I via mTOR Apoptotic Signaling to Inhibit Glioma Cell Growth

Author

Guo,Yangyang, Wang,Cheng, Jiang,Minghui, Zhu,Hengyue, Weng,Min, Sun,Linxiao, and Zhang,Yanlei

Subjects
Cancer Management and Research
Abstract

Yangyang Guo,1,* Cheng Wang,1,* Minghui Jiang,1 Hengyue Zhu,1 Min Weng,1 Linxiao Sun,1 Yanlei Zhang2 1Key Laboratory of Diagnosis and Treatment of Severe Hepato-Pancreatic Diseases of Zhejiang Province, Zhejiang Provincial Top Key Discipline in Surgery, Wenzhou Medical University First Affiliated Hospital, Wenzhou, Zhejiang, People’s Republic of China; 2Neurology Department, Wenzhou Medical University First Affiliated Hospital, Wenzhou, Zhejiang, People’s Republic of China*These authors contributed equally to this workCorrespondence: Yanlei Zhang; Linxiao Sun Email yanlei-zhang@hotmail.com; sunlinxiao@wmu.edu.cnIntroduction: Baohuoside I, a novel oncotherapeutic agent, has been reported to have anti-cancer effects on a variety of cancers, but its role in glioma and its molecular mechanism are still unclear.Methods: The proliferation of U251 cells was detected by real-time cellular analysis (RTCA), CCK-8, Ki67 immunofluorescence and colony formation assay. The effect of Baohuoside I on the invasion and migration of U251 cells was measured by transwell and scratch tests. The apoptosis of U251 cells was detected by flow cytometry. The expression level of related protein was detected by western blotting.Results: Baohuoside I could inhibit the proliferation of human glioma cells and induce apoptosis. Further study showed that the migration and invasion ability of glioma was significantly decreased by Baohuoside I. Western blot revealed the expression of p-AMPKα 1 protein was up-regulated, and the expression of p-mTOR and p-S6K was down-regulated after Baohuoside I treatment. Tumorigenesis in nude mice showed that Baohuoside I had an anti-glioma effect in vivo.Conclusion: We propose a natural product, which can inhibit the proliferation, invasion and migration of glioma and may be a valuable anti-tumor candidate. The inhibitory effect of Baohuoside I on the glioma is achieved by inducing the apoptosis of the tumor cells, rather than autophagy. In addition, the pathway to induce cell apoptosis of Baohuoside I is to target the mTOR signal.Keywords: Baohuoside I, mTOR, glioma, apoptosis, proliferation

Published
2020

29. KRT17 Functions as a Tumor Promoter and Regulates Proliferation, Migration and Invasion in Pancreatic Cancer via mTOR/S6k1 Pathway

Author

Li,Ding, Ni,Xiao-Feng, Tang,Hengjie, Zhang,Jiecheng, Zheng,Chenlei, Lin,Jianhu, Wang,Cheng, Sun,Linxiao, and Chen,Bicheng

Subjects
Cancer Management and Research
Abstract

Ding Li,1,* Xiao-Feng Ni,1,* Hengjie Tang,1,* Jiecheng Zhang,1 Chenlei Zheng,1 Jianhu Lin,1 Cheng Wang,1 Linxiao Sun,1 Bicheng Chen1,2 1Key Laboratory of Diagnosis and Treatment of Severe Hepato-Pancreatic Diseases of Zhejiang Province, Zhejiang Provincial Top Key Discipline in Surgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang Province, People’s Republic of China; 2Department of Clinical Laboratory, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang Province, People’s Republic of China*These authors contributed equally to this workCorrespondence: Bicheng Chen; Linxiao Sun Email chenbicheng@hotmail.com; sunlinxiao@wmu.edu.cnBackground: Pancreatic cancer (PC) is one of the most well-known malignancies with high mortality, but the underlying mechanism of PC remains unknown. Keratin17 (KRT17) expression has been reported in many malignancies, but its functions in PC are not clear. The aim of our study was to evaluate KRT17 expression and its potential role in PC.Methods: The online databases GEPIA and THPA were used to identify KRT17 expression in tissues. Quantitative real-time PCR (qRT-PCR) was used to determine KRT17 expression in cell lines. Ki67 and ROS levels were detected by immunofluorescence assay and a 2ʹ,7ʹ-dichlorodihydrofluorescein diacetate (DCFH-DA) probe. KRT17 downregulation was induced by the small interfering RNA (siRNA) technique. Proliferation function was evaluated by colony formation assay and RTCA. Migration and invasion were evaluated by transwell migration assay. A Western blot assay was used to detect protein levels.Results: KRT17 was overexpressed in PC tissues compared to that in normal tissues. The results showed that Ki67 and ROS levels were decreased in pancreatic cancer cells after transfection with siKRT17. After KRT17 downregulation in PC cell lines, cell viability functions, including proliferation, migration and invasion, and mTOR/S6K1 phosphorylation levels were attenuated.Conclusion: KRT17 knockdown significantly inhibited proliferation, migration and invasion in pancreatic cancer cells.Keywords: KRT17, knockdown, proliferation, migration, invasion, pancreatic cancer, mTOR/S6K1

Published
2020

30. Baohuoside I Inhibits the Proliferation of Pancreatic Cancer Cells via mTOR/S6K1-Caspases/Bcl2/Bax Apoptotic Signaling

Author

Ni, Fubiao, Tang, Hengjie, Wang, Cheng, Zhang, Hewei, Zheng, Chenlei, Zhang, Ning, Chen, Bicheng, and Sun, Linxiao

Subjects
Cancer Management and Research, Baohuoside I, pancreatic cancer, apoptosis, Original Research
Abstract

Fubiao Ni,1,* Hengjie Tang,1,* Cheng Wang,1,* Hewei Zhang,1 Chenlei Zheng,1 Ning Zhang,2 Bicheng Chen,1 Linxiao Sun1 1Key Laboratory of Diagnosis and Treatment of Severe Hepato-Pancreatic Diseases of Zhejiang Province, Zhejiang Provincial Top Key Discipline in Surgery, First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, People’s Republic of China; 2First School of Clinical Medicine, Wenzhou Medical University, Wenzhou, Zhejiang 325000, People’s Republic of China*These authors contributed equally to this workCorrespondence: Linxiao Sun; Bicheng Chen Email sunlinxiao@wmu.edu.cn; bichengchen@hotmail.comBackground: Although the incidence of pancreatic cancer has increased markedly, the 5-year survival rate for this disease is considerably low compared with other types of cancer. Moreover, the mortality rate of pancreatic cancer is similar to its incidence rate. Current therapeutic agents exhibit a lack of specificity for pancreatic cancer. Baohuoside I is traditionally used to treat orgasmic disorder and inflammation. However, its role in pancreatic cancer is unknown.Objective: To explore the effects of Baohuoside I on pancreatic cancer and to study the potential-related molecular mechanism.Materials and methods: In the present study, the antineoplastic effect of Baohuoside I was investigated with regard to pancreatic cancer via colony formation, transwell and migration assay. The energy metabolism changes of pancreatic cancer were tested by flow cytometry analysis and oxidative phosphorylation and glycolysis assay. The target signaling members were analyzed by Western blot.Results: Baohuoside I inhibited the cell growth of pancreatic cancer cells. In addition, it affected intracellular energy metabolism to induce cancer cell apoptosis via the mTOR/S6K1 and the caspase/Bcl2/Bax signaling pathways.Conclusion: The present data provide further insight into the development of novel drugs against pancreatic cancer.Keywords: Baohuoside I, pancreatic cancer, apoptosis

Published
2019

33. Reinventing MoS2 Co-catalytic Fenton reaction: Oxygen-incorporation mediating surface superoxide radical generation.

Author

Tan, Xianjun, Ding, Wenhui, Jiang, Zhenying, Sun, Linxiao, and Huang, Yuxiong

Abstract

To better understand the mechanisms of hydrogen peroxide (H2O2)'s decomposition and reactive oxygen species (ROS)'s formation on the catalyst's surface is always a critical issue for the environmental application of Fenton/Fenton-like reaction. We here report a new approach to activate H2O2 in a co-catalytic Fenton system with oxygen incorporated MoS2, namely MoS2−xOx nanosheets. The MoS2−xOx nanosheets assisted co-catalytic Fenton system exhibited superior degradation activity of emerging antibiotic contaminants (e.g., sulfamethoxazole). Combining density functional theory (DFT) calculation and experimental investigation, we demonstrated that oxygen incorporation could improve the intrinsic conductivity of MoS2−xOx nanosheets and accelerate surface/interfacial charge transfer, which further leads to the efficacious activation of H2O2. Moreover, by tuning the oxygen proportion in MoS2−xOx nanosheets, we are able to modulate the generation of ROS and further direct the oriented-conversion of H2O2 to surface-bounded superoxide radical (·O2 surface−). It sheds light on the generation and transformation of ROS in the engineered system (e.g., Fenton, Fenton-like reaction) for efficient degradation of persistent pollutants. [ABSTRACT FROM AUTHOR]

Published
2022
Full Text
View/download PDF

42. Berzosertib (VE-822) inhibits gastric cancer cell proliferation via base excision repair system

Author

Ni, Fubiao, Tang, Hengjie, Wang, Cheng, Wang, Zixiang, Yu, Fangyi, Chen, Bicheng, and Sun, Linxiao

Subjects
Cancer Management and Research, gastric cancer, base excision repair, Kaplan-Meier plotter, Original Research
Abstract

Fubiao Ni,1,* Hengjie Tang,1,* Cheng Wang,1,* Zixiang Wang,2 Fangyi Yu,2 Bicheng Chen,1 Linxiao Sun1 1Key Laboratory of Diagnosis and Treatment of Severe Hepato-Pancreatic Diseases of Zhejiang Province, Zhejiang Provincial Top Key Discipline in Surgery, First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, People’s Republic of China; 2First College of Clinical Medicine, Wenzhou Medical University, Wenzhou, Zhejiang, People’s Republic of China*These authors contributed equally to this workCorrespondence: Linxiao SunKey Laboratory of Diagnosis and Treatment of Severe Hepato-Pancreatic Diseases of Zhejiang Province, Zhejiang Provincial Top Key Discipline in Surgery, First Affiliated Hospital of Wenzhou MedicalUniversity, Fanhai West Road, Nanbaixiang Street, Wenzhou 325006, Zhejiang, People’s Republic of ChinaEmail sunlinxiao@wmu.edu.cnnBackground: Current investigations suggest that the Base Excision Repair (BER) system may change DNA repair capacity and affect clinical gastric cancer progression such as overall survival. However, the prognostic value of BER system members in gastric cancer remains unclear.Methods: We explored the prognostic correlation between 7 individual BER genes, including uracil-DNA glycosylase (UNG), Single-strand-selective monofunctional uracil-DNA glycosylase 1 (SMUG1), Methyl-CpG binding domain 4 (MBD4), thymine DNA glycosylase (TDG), 8-oxoguanine DNA glycosylase (OGG1), MutY DNA glycosylase (MUTYH) and Nei like DNA glycosylase 1 (NEIL1), expression and overall survival (OS) in different clinical data, such as Lauren classification, pathological stages, human epidermal growth factor receptor-2 (HER2) expression status, treatment strategy, gender and differentiation degree in gastric cancer patients, using Kaplan-Meier plotter (KM plotter) online database. Based on the bioinformatics analysis, we utilized Berzosertib (VE-822) to inhibit DNA damage repair in cancer cells compared to solvent control group via real-time cellular analysis (RTCA), flow cytometry, colony formation and migration assay. Finally, we utilized reverse transcription-polymerase chain reaction (RT-PCR) to confirm the expression of BER members between normal and two gastric cancer cells or solvent and VE-822 treated groups.Results: Our work revealed that high UNG mRNA expression was correlated with high overall survival probability; however, high SMUG1, MBD4, TDG, OGG1, MUTYH and NEIL1 mRNA expression showed relatively low overall survival probability in all GC patients. Additionally, UNG was associated with high overall survival probability in intestinal and diffuse types, but SMUG1 and NEIL1 showed opposite results. Further, VE-822 pharmacological experiment suggested that inhibition of DNA damage repair suppressed gastric cancer cells’ proliferation and migration ability via inducing apoptosis. Further, real-time polymerase chain reaction results proposed the inhibition of gastric cancer cells by VE-822 may be through UNG, MUTYH and OGG-1 of BER system.Conclusion: We comprehensively analyze the prognostic value of the BER system (UNG, SMUG1, MBD4, TDG, OGG1, MUTYH and NEIL1) based on bioinformatics analysis and experimental confirmation. BER members are associated with distinctive prognostic significance and maybe new valuable prognostic indicators in gastric cancer.Keywords: base excision repair, gastric cancer, Kaplan-Meier plotter

Published
2019

43. Emerging investigator series: hetero-phase junction 1T/2H-MoS2nanosheets decorated by FeOOH nanoparticles for enhanced visible light photo-Fenton degradation of antibioticsElectronic supplementary information (ESI) available. See DOI: https://doi.org/10.1039/d2en00045h

Author

Sun, Linxiao, Tan, Xianjun, Ding, Wenhui, and Huang, Yuxiong

Abstract

The photo-Fenton system is considered to be an economical and environmentally-friendly way to remove organic pollutants in the aquatic environment. However, slow electron transfer and retarded Fe2+/Fe3+conversion have hampered its practical applications. Herein, we designed and prepared the hetero-phase junction 1T/2H-MoS2@FeOOH, effectively enhancing the photo-Fenton degradation efficiency by 3.25-fold compared to FeOOH alone. Theoretical calculations demonstrated that the 1T/2H-MoS2hetero-phase junction features mid-gap states and a narrower band gap, enabling broader visible-light absorption and quicker electron transport. Additionally, the application of 1T/2H-MoS2@FeOOH resulted in Fe2+/Fe3+and Mo4+/Mo6+dual reaction sites, which were beneficial for the sufficient activation of H2O2to HO2. HO2-dominated degradation pathways and mechanisms were revealed to provide new insights for developing advanced oxidation processes to effectively remove emerging contaminants.

Published
2022
Full Text
View/download PDF

45. Periplocin inhibits the growth of pancreatic cancer by inducing apoptosis via AMPK‐mTOR signaling.

Author

Xie, Gangyin, Sun, Linxiao, Li, Yonglin, Chen, Bicheng, and Wang, Cheng

Subjects
*PANCREATIC cancer, *TUMOR growth, *CANCER cell proliferation, *CELL migration, *APOPTOSIS
Abstract

Background: Periplocin is a monomeric compound that exhibits anti‐tumor activities. It is extracted from Cortex Periplocae. Objective: This study aimed at determining the effect of periplocin treatment on the apoptosis and proliferation of human pancreatic cancer cells, and to elucidate on its mechanisms of action. Methods: PANC1 and cfpac1 cells were treated with periplocin. Cell proliferation was detected by RTCA, Ki67 immunofluorescence, and a clonogenic assay. The transwell assay was used to examine cell migration and invasion functions. The expression of apoptosis‐associated proteins was detected by flow cytometry and western blotting. Total RNA was extracted from the treated and untreated group of PANC1 cells for RNA‐seq detection and analysis. Differentially expressed genes were screened for GO biological process and KEGG pathway analysis. Finally, CFPAC1 cells were subcutaneously inoculated into BALB / c nude mice to assess tumor growth. Results: Periplocin inhibited the proliferation of PANC1 and CFPAC1 cells and induced their apoptosis by activating the AMPK/mTOR pathway and inhibiting p70 S6K. It also attenuated the cell migration, invasion, and inhibited the growth of cfpac1 xenografts in nude mice. Conclusions: Periplocin inhibits human pancreatic cancer cell proliferation and induces their apoptosis by activating the AMPK / mTOR pathway. [ABSTRACT FROM AUTHOR]

Published
2021
Full Text
View/download PDF

48. LC-Q-TOF-MS Characterization of Polyphenols from White Bayberry Fruit and Its Antidiabetic Effect in KK-A y Mice.

Author

Liu Y, Zhang X, Zhan L, Xu C, Sun L, Jiang H, Sun C, and Li X

Abstract

The present study is to investigate the polyphenolic composition and in vivo antidiabetic effect of white-fleshed Chinese bayberry cultivar "Shui Jing". By liquid chromatography quadrupole time-of-flight mass spectrometry (LC-Q-TOF-MS), 38 polyphenols were identified in the Shui Jing fruit extract (SJE), where proanthocyanidins (PAs), including epigallocatechin gallate (EGCG), as well as flavonols, including myricitrin and quercetrin, were the predominant ingredients. After a 5-week experiment, the SJE (200 mg/kg bodyweight) significantly reduced fasting blood glucose, elevated glucose tolerance, and insulin sensitivity in diabetic KK-A y mice. It markedly attenuated bodyweight gain and decreased glycolipid metabolism-related markers including insulin, leptin, glucagon, triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-c) and alanine aminotransferase (ALT) levels in mice. Liver weight and hepatic lipid accumulation were also significantly reduced by the SJE. Gene expressions of insulin 1 ( INS1 ) and glycogen synthase kinase 3 β ( GSK3b ) were markedly inhibited while the hepatic phosphorylation of AMPKα was significantly increased in the liver of SJE-treated mice, indicating that the SJE may exert an antidiabetic effect through an AMPK-dependent pathway. In conclusion, white bayberry rich in PAs and flavonols may have great potential in the regulation of diabetes mellitus., Competing Interests: The authors declare no competing financial interest., (Copyright © 2020 American Chemical Society.)

Published
2020
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results