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31 results on '"Yan, Xueqin"'

1. Current Views on Mechanisms of the FLASH Effect in Cancer Radiotherapy

Author

Ma, Yuqi, Zhao, Ziming, Zhang, Wenkang, Lv, Jianfeng, Chen, Junyi, Yan, Xueqin, Lin, XiaoJi, Zhang, Junlong, Wang, Bingwu, Gao, Song, Xiao, Jie, and Yang, Gen

Subjects
Physics - Medical Physics
Abstract

FLASH radiotherapy (FLASH-RT) is a new modality of radiotherapy by delivering doses with ultra-high dose rates. FLASH-RT has the ability to suppress tumor growth while sparing normal tissues, known as the FLASH effect. Although FLASH effect has proved valid in various models by different ionizing radiations, the exact underlying mechanism is still unclear. This article summarizes mainstream hypotheses of FLASH effect at physicochemical and biological levels, including oxygen depletion and free radical reactions, nuclear and mitochondria damage, as well as immune response. These hypotheses contribute reasonable explanations to the FLASH effect, and are interconnected according to the chronological order of the organism's response to ionizing radiation. By collating the existing consensus, evidence, and hypotheses, this article provides a comprehensive overview of potential mechanisms of FLASH effect and practical guidance for future investigation in the field of FLASH-RT., Comment: 24 pages, 5 figures

Published
2024

2. Validation of an AI-Powered Automated X-ray Bone Age Analyzer in Chinese Children and Adolescents: A Comparison with the Tanner–Whitehouse 3 Method

Author

Liang, Yan, Chen, Xiaobo, Zheng, Rongxiu, Cheng, Xinran, Su, Zhe, Wang, Xiumin, Du, Hongwei, Zhu, Min, Li, Guimei, Zhong, Yan, Cheng, Shengquan, Yu, Baosheng, Yang, Yu, Chen, Ruimin, Cui, Lanwei, Yao, Hui, Gu, Qiang, Gong, Chunxiu, Jun, Zhang, Huang, Xiaoyan, Liu, Deyun, Yan, Xueqin, Wei, Haiyan, Li, Yuwen, Zhang, Huifeng, Liu, Yanjie, Wang, Fengyun, Zhang, Gaixiu, Fan, Xin, Dai, Hongmei, and Luo, Xiaoping

Published
2024
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9. A comprehensive diagnostic of liquid sheet targets for laser ion acceleration

Author

Peng, Ziyang, primary, Cao, Zhengxuan, additional, Liu, Xuan, additional, Shou, Yinren, additional, Zhao, Jiarui, additional, Chen, Shiyou, additional, Gao, Ying, additional, Wang, Pengjie, additional, Mei, Zhusong, additional, Pan, Zhuo, additional, Kong, Defeng, additional, Xu, Shirui, additional, Liu, Zhipeng, additional, Liang, Yulan, additional, Xu, Tianqi, additional, Song, Tan, additional, Chen, Xun, additional, Wu, Qingfan, additional, Zhang, Yujia, additional, Zhang, Zihao, additional, Yan, Xueqin, additional, and Ma, Wenjun, additional

Published
2024
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13. TH-4000, a hypoxia-activated pan-HER inhibitor, shows excellent preclinical efficacy for the treatment of HER2+ breast cancer.

Author

Shao, Xinyi, Yang, Dawei, Shan, Liuqun, Yan, Xueqin, Xu, Di, Li, Lei, Sun, Yidan, Yu, Qiang, Zhou, Honglei, Ding, Yongbin, and Tang, Jinhai

Subjects
BREAST cancer, POISONS, PROTEIN-tyrosine kinase inhibitors, HER2 positive breast cancer, MONOCLONAL antibodies, EPIDERMAL growth factor receptors, REACTIVE oxygen species
Abstract

Human epidermal growth factor receptor 2-positive (HER2+) breast cancer is correlated with poor prognosis, the current treatment of which is still based on surgery and adjuvant targeted therapy with monoclonal antibody. Problems of drug resistance hinder the use of monoclonal antibodies. Subsequently, tyrosine kinase inhibitors (TKIs) have been noticed, TKIs have the advantages of multi-targets and reduced drug resistance. However, TKIs that target HER family proteins often cause adverse effects such as liver damage and diarrhea. Thus, TKIs with high selectivity are being developed. TH-4000, a prodrug that generated an active form TH-4000Effector (TH-4000E) under hypoxic condition, was evaluated in this research. We found that TH-4000E ([(E)-4-[[4-(3-bromo-4-chloroanilino)pyrido[3,4-d]pyrimidin-6-yl]amino]-4-oxobut-2-enyl]-dimethyl-[(3-methyl-5-nitroimidazol-4-yl)methyl]azanium) (1–1000 nM) had potent and highly selective toxic effects on HER2+ breast cancer cells and inhibited the phosphorylation of HER family kinases at lower doses than that of Lapatinib and Tucatinib. TH-4000E activated Caspase-3 and induced apoptosis through a reactive oxygen species (ROS)-dependent pathway. The prodrug TH-4000 ([(E)-4-[[4-(3-bromo-4-chloroanilino)pyrido[3,4-d]pyrimidin-6-yl]amino]-4-oxobut-2-enyl]-dimethyl-[(3-methyl-5-nitroimidazol-4-yl)methyl]azanium;bromide) (50 mg/kg) effectively suppressed the tumor growth with less liver damage in mouse tumor models. This hypoxia-targeted strategy has possessed advantage in avoiding drug-induced liver damage, TH-4000 could be a promising drug candidate for the treatment of HER2+ breast cancer. [ABSTRACT FROM AUTHOR]

Published
2024
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15. A novel colchicine-myricetin heterozygous molecule: design, synthesis, and effective evaluations on the pathological models of acute lung injury in vitro and in vivo

Author

Li, Zhiyue, primary, Yan, Xueqin, additional, Wei, Jiangchun, additional, Pu, Liuyang, additional, Zhu, Guanbao, additional, Cao, Yongkai, additional, Liu, Zhanyan, additional, Liu, Yaqian, additional, Li, Yan, additional, Li, Limin, additional, Li, Xinping, additional, and Wu, Zhengzhi, additional

Published
2023
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20. USP38 inhibits colorectal cancer cell proliferation and migration via downregulating HMX3 ubiquitylation

Author

Wang, Jun, Gu, Yongxing, Yan, Xueqin, Zhang, Jie, and Ding, Yong

Abstract

Accumulating evidence has shown that H6 Family Homeobox 3 (HMX3) plays a crucial role in nervous system regulation. However, the regulatory mechanism of HMX3 in colorectal cancer (CRC) has seldom been studied. Herein, HMX3 was significantly downregulated in CRC, as demonstrated by qRT-PCR and WB analysis on clinical samples and a panel of cell lines. Besides, it was found that the expression of HMX3 was negatively correlated with survival of CRC patients. The functional analyses (EdU staining, CCK-8, colony formation, Transwell, and wound scratch assays) showed that CRC cell proliferation, migration, and invasion were significantly suppressed by HMX3 overexpression, while enhanced by HMX3 knockdown. Moreover, in vivo experiment revealed HMX3 overexpression could also suppress tumor growth. Combining bioinformatics and WB analysis, we preliminarily uncovered that HMX3 was involved in apoptosis and KRAS signaling pathways. Mechanistically, Ubiquitin-specific protease 38 (USP38) was identified as a novel post-translational regulator of HMX3, which could directly interact with HMX3 to stabilize its protein expression via deubiquitination. Furthermore, the role of USP38 silencing in promoting cell proliferation, migration, and invasion of CRC cells was blocked by HMX3 overexpression. In conclusion, our findings suggested that USP38/HMX3 axis is a novel promising therapeutic candidate for CRC.

Published
2022
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21. USP38 inhibits colorectal cancer cell proliferation and migration via downregulating HMX3 ubiquitylation

Author

Wang, Jun, Gu, Yongxing, Yan, Xueqin, Zhang, Jie, Wang, Jun, and Ding, Yong

Abstract

ABSTRACTAccumulating evidence has shown that H6 Family Homeobox 3 (HMX3) plays a crucial role in nervous system regulation. However, the regulatory mechanism of HMX3 in colorectal cancer (CRC) has seldom been studied. Herein, HMX3 was significantly downregulated in CRC, as demonstrated by qRT-PCR and WB analysis on clinical samples and a panel of cell lines. Besides, it was found that the expression of HMX3 was negatively correlated with survival of CRC patients. The functional analyses (EdU staining, CCK-8, colony formation, Transwell, and wound scratch assays) showed that CRC cell proliferation, migration, and invasion were significantly suppressed by HMX3 overexpression, while enhanced by HMX3 knockdown. Moreover, in vivoexperiment revealed HMX3 overexpression could also suppress tumor growth. Combining bioinformatics and WB analysis, we preliminarily uncovered that HMX3 was involved in apoptosis and KRAS signaling pathways. Mechanistically, Ubiquitin-specific protease 38 (USP38) was identified as a novel post-translational regulator of HMX3, which could directly interact with HMX3 to stabilize its protein expression via deubiquitination. Furthermore, the role of USP38 silencing in promoting cell proliferation, migration, and invasion of CRC cells was blocked by HMX3 overexpression. In conclusion, our findings suggested that USP38/HMX3 axis is a novel promising therapeutic candidate for CRC.

Published
2023
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22. Glycated Haemoglobin A1c Variability Score Elicits Kidney Function Decline in Chinese People Living with Type 2 Diabetes.

Author

Zhou, Yiling, Huang, Hongmei, Yan, Xueqin, Hapca, Simona, Bell, Samira, Qu, Furong, Liu, Li, Chen, Xiangyang, Zhang, Shengzhao, Shi, Qingyang, Zeng, Xiaoxi, Wang, Miye, Li, Nan, Du, Heyue, Meng, Wentong, Su, Baihai, Tian, Haoming, and Li, Sheyu

Subjects
TYPE 2 diabetes, KIDNEY physiology, CHINESE people, HEMOGLOBINS, GLOMERULAR filtration rate
Abstract

Our aim was to investigate the association of glycated haemoglobin A1c (HbA1c) variability score (HVS) with estimated glomerular filtration rate (eGFR) slope in Chinese adults living with type 2 diabetes. This cohort study included adults with type 2 diabetes attending outpatient clinics between 2011 and 2019 from a large electronic medical record-based database of diabetes in China (WECODe). We estimated the individual-level visit-to-visit HbA1c variability using HVS, a proportion of changes in HbA1c of ≥0.5% (5.5 mmol/mol). We estimated the odds of people experiencing a rapid eGFR annual decline using a logistic regression and differences across HVS categories in the mean eGFR slope using a mixed-effect model. The analysis involved 2397 individuals and a median follow-up of 4.7 years. Compared with people with HVS ≤ 20%, those with HVS of 60% to 80% had 11% higher odds of experiencing rapid eGFR annual decline, with an extra eGFR decline of 0.93 mL/min/1.73 m2 per year on average; those with HVS > 80% showed 26% higher odds of experiencing a rapid eGFR annual decline, with an extra decline of 1.83 mL/min/1.73 m2 per year on average. Chinese adults with type 2 diabetes and HVS > 60% could experience a more rapid eGFR decline. [ABSTRACT FROM AUTHOR]

Published
2022
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25. Dihydroartemisinin inhibits EMT induced by platinum-based drugs via Akt-Snail pathway

Author

Weilong Zhong, Denghui Zhai, Cheng Yang, Jia-Huan Yang, Honggang Zhou, Yan Xueqin, Guang Yang, Yuan Qin, Tao Sun, Meng Li, Huijuan Liu, Shuang Chen, Kailiang Qiao, and Wei Yang

Subjects
0301 basic medicine, Drug, endocrine system diseases, medicine.medical_treatment, media_common.quotation_subject, Dihydroartemisinin, Drug resistance, dihydroartemisinin, 03 medical and health sciences, 0302 clinical medicine, In vivo, medicine, Protein kinase B, media_common, Chemotherapy, Chemistry, Akt, EMT, Oxaliplatin, 030104 developmental biology, Snail, Oncology, 030220 oncology & carcinogenesis, Cancer cell, Cancer research, Research Paper, medicine.drug
Abstract

Artemisinin and its derivatives exhibit a high activity against a range of cancer cell types both in vitro and in vivo. In clinical practice, platinum-based anti-cancer chemotherapy is widely used to treat tumors. However, a large proportion of patients receiving these treatments will relapse because of metastasis and drug resistance. The purpose of this study is to explore the combinational anti-metastatic effect of platinum-based drugs and dihydroartemisinin (DHA). Both DDP and oxaliplatin (OXA) at low doses could induce epithelial–mesenchymal transition (EMT) in HCC. Meanwhile, co-administration of DHA could enhance DDP and OXA chemosensitivity in HCC and reverse drug resistance. DHA reversed the morphological changes induced by DDP or OXA and reversed the changes in EMT biomarkers induced by DDP and OXA in HCC in vitro and in vivo via AKT–Snail signaling. DHA significantly increased platinum-based drug sensitivity and suppressed EMT induced by platinum-based drugs via AKT–Snail signaling in HCC. DHA is expected to become the new adjuvant for chemotherapy.

Published
2017

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