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17 results on '"Qu, JunWei"'

2. Biotin attenuates heat shock factor 4b transcriptional activity by lysine 444 biotinylation

Author

Yan, Longjun, primary, Li, Jing, additional, Hu, Jialin, additional, Qu, Junwei, additional, Li, Kejia, additional, Wang, Mingli, additional, An, Shuang-Shuang, additional, Ke, Cun-cun, additional, Li, Hui, additional, Yuan, Fengling, additional, Guo, Weikai, additional, Hu, Mengyue, additional, Zhang, Jing, additional, Yang, Zhengyan, additional, Mu, Hongmei, additional, zhang, Fengyan, additional, Zhang, Jun, additional, Cui, Xiukun, additional, and Hu, Yanzhong, additional

Published
2022
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6. FcRn is not the receptor mediating the transfer of serum IgG to colostrum in pigs

Author

Ke, Cuncun, primary, Ma, Yonghe, additional, Pan, Dengke, additional, Wan, Zihui, additional, Feng, Tao, additional, Yu, Dawei, additional, Liu, Xiaojuan, additional, Wang, Haitao, additional, Du, Minjie, additional, Huang, Linhua, additional, Zhang, Yifu, additional, Du, Lijuan, additional, Wang, Xifeng, additional, Li, Kongpan, additional, Yu, Di, additional, Zhang, Ming, additional, Huang, Jinwei, additional, Qu, Junwei, additional, Ren, Liming, additional, Hu, Yanzhong, additional, Cao, Gengsheng, additional, Hu, Xiaoxiang, additional, Wu, Sen, additional, Han, Haitang, additional, and Zhao, Yaofeng, additional

Published
2021
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7. Monoclonal antibody AC10364 inhibits cell proliferation in 5-fluorouracil resistant hepatocellular carcinoma via apoptotic pathways

Author

Wu, Jianzhong, Qu, Junwei, Cao, Haixia, Jing, Changwen, Wang, Zhuo, Xu, Heng, and Ma, Rong

Subjects
monoclonal antibody, apoptosis, inhibitory, genes, OncoTargets and Therapy, Original Research
Abstract

Jianzhong Wu,1,* Junwei Qu,1,* Haixia Cao,1 Changwen Jing,1 Zhuo Wang,1 Heng Xu,2 Rong Ma11Research Center for Clinical Oncology, Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research, Nanjing Medical University Affiliated Cancer Hospital, Nanjing, Jiangsu 210000, People’s Republic of China; 2Laboratory of Pharmaceutical Chemistry, Jiangsu Province Institute of Materia Medica, Nanjing Tech University, Nanjing, Jiangsu 211816, People’s Republic of China*These authors contributed equally to this work Background: This study was designed to investigate the antitumor activity of the mAb (AC10364) in vitro and elucidate the related mechanisms of inhibition to cell growth using bel/fu cells treated with AC10364. Methods: The inhibitory effects of AC10364 on the proliferation of Bel/fu cells were examined using a cytotoxicity assay. Apoptosis of Bel/fu cells was detected using FITC annexin V and PI staining following treatment with AC10364 for 24h. The factors regulating apoptosis were identified by Western blot using lysates of Bel/fu cells treated with AC10364 for 0, 12, 24, or 36h. Genes associated with tumorigenesis or growth were analyzed by reverse transcription–quantitative polymerase chain reaction using Bel/fu cells treated for 12, 24, or 36h with AC10364. Results: The early apoptotic ratios of Bel/fu cells treated with AC10364 increased in a dose-dependent manner. The levels of caspases, including cleaved caspase-3, caspase-3 and caspase-9, were significantly high in Bel/fu cells treated with AC10364 (P

Published
2019

8. Monoclonal antibody AC10364 inhibits cell proliferation in 5-fluorouracil resistant hepatocellular carcinoma via apoptotic pathways

Author

Wu,JianZhong, Qu,JunWei, Cao,HaiXia, Jing,ChangWen, Wang,Zhuo, Xu,Heng, Ma,Rong, Wu,JianZhong, Qu,JunWei, Cao,HaiXia, Jing,ChangWen, Wang,Zhuo, Xu,Heng, and Ma,Rong

Abstract

Jianzhong Wu,1,* Junwei Qu,1,* Haixia Cao,1 Changwen Jing,1 Zhuo Wang,1 Heng Xu,2 Rong Ma11Research Center for Clinical Oncology, Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research, Nanjing Medical University Affiliated Cancer Hospital, Nanjing, Jiangsu 210000, People’s Republic of China; 2Laboratory of Pharmaceutical Chemistry, Jiangsu Province Institute of Materia Medica, Nanjing Tech University, Nanjing, Jiangsu 211816, People’s Republic of China*These authors contributed equally to this work Background: This study was designed to investigate the antitumor activity of the mAb (AC10364) in vitro and elucidate the related mechanisms of inhibition to cell growth using bel/fu cells treated with AC10364. Methods: The inhibitory effects of AC10364 on the proliferation of Bel/fu cells were examined using a cytotoxicity assay. Apoptosis of Bel/fu cells was detected using FITC annexin V and PI staining following treatment with AC10364 for 24 h. The factors regulating apoptosis were identified by Western blot using lysates of Bel/fu cells treated with AC10364 for 0, 12, 24, or 36 h. Genes associated with tumorigenesis or growth were analyzed by reverse transcription–quantitative polymerase chain reaction using Bel/fu cells treated for 12, 24, or 36 h with AC10364. Results: The early apoptotic ratios of Bel/fu cells treated with AC10364 increased in a dose-dependent manner. The levels of caspases, including cleaved caspase-3, caspase-3 and caspase-9, were significantly high in Bel/fu cells treated with AC10364 (P<0.001). Compared with untreated cells, those exposed to AC10364 had showed significant downregulation of the expression of binding protein gene (G protein subunit α 15, GNA15) and other protein-coding genes, including fms-related tyrosine kinase 1(FLT1), nicotinamide phosphoribosyltransferase (NAMPT), netrin 4 (NTN4), platelet-derived growth factor subunit A (PDGFA), S100

Published
2019

9. The Higher Response of Vascular Endothelial Growth Factor and Angiotensin-II to Human Chorionic Gonadotropin in Women with Polycystic Ovary Syndrome

Author

Qu, Junwei, Che, Yena, Xu, Pei, Xia, Yanjie, Wu, Xiaoke, and Wang, Yong

Subjects
lcsh:R5-920, Gynecology and Female Infertility, endocrine system diseases, vascular endothelial growth factor, polycystic ovary syndrome, ovarian hyperstimulation syndrome, Angiotensin-II, Original Article, angiotensin, ii, lcsh:Medicine (General), female genital diseases and pregnancy complications, Endocrinology and Metabolism
Abstract

Background: This research investigated the response of vascular active factors, vascular endothelial growth factor (VEGF) and angiotensin-II (AT-II) to ovarian stimulation during 24 hours in patients with polycystic ovary syndrome (PCOS). Materials and Methods: In this clinical trial study, 52 patients with PCOS and 8 control cases were stimulated with human chorionic gonadotropin (HCG) on the 4th to 7th day of the patients’ natural or induced menstrual cycles. We measured VEGF and AT-II by radioimmunoassay before the injection (0 hour) and 3, 8, 12, 18 and 24 hours after the stimulation. Results: After ovarian stimulation, there was substantially higher level of VEGF in typical PCOS patients than the other three groups at the 3 hour time point (p

Published
2015

11. SNAP23 promotes the malignant process of ovarian cancer

Author

Sun, Qi, primary, Huang, Xing, additional, Zhang, Quanli, additional, Qu, Junwei, additional, Shen, Yang, additional, Wang, Xin, additional, Sun, Haijun, additional, Wang, Jie, additional, Xu, Lin, additional, Chen, Xiaoxiang, additional, and Ren, Binhui, additional

Published
2016
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17. SNAP23 suppresses cervical cancer progression via modulating the cell cycle.

Author

Lu, Emei, Zhu, Biqing, Wu, Yaqin, Zhang, Quanli, Zheng, Xiufen, Luo, Jing, Xu, Lin, Ren, Binhui, and Qu, Junwei

Subjects
*CERVICAL cancer, *CELL cycle, *PROGNOSIS, *TUMOR suppressor genes, *GENETIC overexpression, *SMALL interfering RNA
Abstract

Objective Cervical cancer (CC) is one of the most common gynecologic tumors in women worldwide, with poor prognosis and low survival rate. In this study, we identified SNAP23 as a potential tumor suppressor gene in CC. Methods The expression of SNAP23 in tissues and cell lines were measured by qRT-PCR, western blot and IHC. Knockdown of SNAP23 by siRNA and ectopic expression of SNAP23 by overexpression plasmid were performed to observe the biological function of SNAP23 in CC. Xenograft nude mice models were established to measure its function in vivo. Results SNAP23 was downregulated in CC tissues and had a negative correlation with advanced clinical characteristics. Ectopic expression of SNAP23 suppressed malignant phonotype of CC while knockdown of SNAP23 promoted the progression of CC in vitro. The flow cytometry analysis revealed that SNAP23 exerted its tumor suppressor activity via inducing G2/M cell cycle arrest. Moreover, xenograft tumor models showed that SNAP23 suppresses tumor growth in vivo. Conclusions Our results revealed that SNAP23 suppressed progression of CC and induced cell cycle G2/M arrest via upregulating p21 cip1 and downregulating CyclinB1. [ABSTRACT FROM AUTHOR]

Published
2018
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