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| 1 | Melatonin enhances radiofrequency-induced NK antitumor immunity,causing cancer metabolism reprogramming and inhibition of multiple pulmonary tumor development显示文摘Surgery is the comm on treatme nt for early lung cancer with multiple pulm onary no dules,but it is often accompanied by the problem of significant malignancy of other nodules in non-therapeutic areas.In this study,we found that a combined treatment of local rad iofreq ue ncy ablati on(RFA)and melatonin(MLT)greatly improved clinical outcomes for early lung cancer patie nts with multiple pulmonary nodules by minimizing lung function injury and reducing the probability of malignant transformation or enlargement of nodules in non-ablated areas.Mechanically,as demonstrated in an associated mouse lung tumor model,RFA not only effectively remove treated tumors but also stimulate antitumor immunity,which could inhibit tumor growth in non-ablated areas.MLT enhanced RFA-stimulated NK activity and exerted synergistic antitumor effects with RFA.Transcriptomics and proteomics analyses of residual tumor tissues revealed enhanced oxidative phosphorylation and reduced acidification as well as hypoxia in the tumor microenvironment,which suggests reprogrammed tumor metabolism after combined treatment with RFA and MLT.Analysis of residual tumor further revealed the depressed activity of MAPK,NF-kappa B,Wnt,and Hedgehog pathways and upregulated P53 pathway in tumors,which was in line with the inhibited tumor growth.Combined RFA and MLT treatment also reversed the Warburg effect and decreased tumor malignancy.These findings thus demonstrated that combined treatment of RFA and MLT effectively inhibited the malignancy of non-ablated nodules and provided an innovative non-invasive strategy for treating early lung tumors with multiple pulmonary nodules.Trial registration:www.chictr.org.cn,identifier ChiCTR2100042695,http://gffzz62a03ee25e6f4a77h5o0uk69kwq666wko.ffgz.tsg.suse.edu.cn/showproj.aspx?proj=120931. | Ming Li Bingjie Hao Menghuan Zhang Russel J.Reiter Shumeng Lin Tiansheng Zheng Xiangyun Chen Yanbei Ren Liduo Yue Baigenzhin Abay Guojie Chen Xiao Xu Yufeng Shi Lihong Fan | 2021 | Signal Transduction and Targeted Therapy2021，6，10： | 6 |
| 2 | Imbalance of the reciprocally inhibitory loop between the ubiquitin-specific protease USP43 and EGFR/PI3K/AKT drives breast carcinogenesis显示文摘 | Lin He Xinhua Liu Jianguo Yang Wanjin Li Shumeng Liu Xujun Liu Ziran Yang Jie Ren Yue Wang Lin Shan Chengjian Guan Fei Pei Liandi Lei Yu Zhang Xia Yi Xiaohan Yang Jing Liang Rong Liu Luyang Sun Yongfeng Shang | 2018 | Cell Research2018，28，9： | 5 |
| 3 | Dual inhibition of glycolysis and oxidative phosphorylation by aptamer-based artificial enzyme for synergistic cancer therapy显示文摘Dual inhibition of glycolysis and oxidative phosphorylation(OXPHOS)can break the metabolic plasticity of cancer cells to inhibit most energy supply and lead to effective cancer therapy.However,the pharmacokinetic difference among drugs hinders these two inhibitions to realize a uniform temporal and spatial distribution.Herein,we report an aptamer-based artificial enzyme for simultaneous dual inhibition of glycolysis and OXPHOS,which is constructed by arginine aptamer modified carbon-dots-doped graphitic carbon nitride(AptCCN).AptCCN can circularly capture intracellular arginine attribute to the specific binding ability of arginine aptamers to arginine,and further catalyze the oxidation of enriched arginine to nitric oxide(NO)under red light irradiation.In vitro and in vivo experiments showed that arginine depletion and NO stress could inhibit glycolysis and OXPHOS,leading to energy blockage and apoptosis of cancer cells.The presented aptamer-based artificial enzyme strategy provides a new path for cell pathway regulation and synergistic cancer therapy. | Xiao Fang Meng Yuan Junduan Dai Qianying Lin Yuhong Lin Wenli Wang Yifan Jiang Haihui Wang Fang Zhao Junye Wu Shumeng Bai Chunhua Lu Huanghao Yang | 2022 | Nano Research2022，15，7： | 0 |
| 4 | The existence of a nonclassical TCA cycle in the nucleus that wires the metabolic-epigenetic circuitry显示文摘The scope and variety of the metabolic intermediates from the mitochondrial tricarboxylic acid(TCA)cycle that are engaged in epigenetic regulation of the chromatin function in the nucleus raise an outstanding question about how timely and precise supply/consumption of these metabolites is achieved in the nucleus.We report here the identification of a nonclassical TCA cycle in the nucleus(nTCA cycle).We found that all the TCA cycle-associated enzymes including citrate synthase(CS),aconitase 2(ACO2),isocitrate dehydrogenase 3(IDH3),oxoglutarate dehydrogenase(OGDH),succinyl-CoA synthetase(SCS),fumarate hydratase(FH),and malate dehydrogenase 2(MDH2),except for succinate dehydrogenase(SDH),a component of electron transport chain for generating ATP,exist in the nucleus.We showed that these nuclear enzymes catalyze an incomplete TCA cycle similar to that found in cyanobacteria.We propose that the nTCA cycle is implemented mainly to generate/consume metabolic intermediates,not for energy production.We demonstrated that the nTCA cycle is intrinsically linked to chromatin dynamics and transcription regulation.Together,our study uncovers the existence of a nonclassical TCA cycle in the nucleus that links the metabolic pathway to epigenetic regulation. | Xujun Liu Wenzhe Si Lin He Jianguo Yang Yani Peng Jie Ren Xiaoping Liu Tong Jin Huajing Yu Zihan Zhang Xiao Cheng Wenting Zhang Lu Xia Yunchao Huang Yue Wang Shumeng Liu Lin Shan Yu Zhang Xiaohan Yang Haixia Li Jing Liang Luyang Sun Yongfeng Shang | 2021 | Signal Transduction and Targeted Therapy2021，6，12： | 0 |
| 5 | CDYL作为丁烯酰辅酶A水合酶调控组蛋白丁烯酰化及精子发生显示文摘文章简介本研究发现,转录辅抑制因子CDYL具有负调控组蛋白赖氨酸丁烯酰化的功能。有趣的是,CDYL负调控组蛋白丁烯酰化并不是通过直接从底物赖氨酸上去除丁烯酰基的方式实现的,而是利用CDYL的丁烯酰辅酶A水合酶活性。 | Shumeng Liu Huajing Yu Yongqing Liu Xinhua Liu Yu Zhang Chen Bu Shuai Yuan Zhe Chen Guojia Xie Wanjin Li Bosen Xu Jianguo Yang Lin He Tong Jin Yundong Xiong Luyang Sun Xiaohui Liu Chunsheng Han Zhongyi Cheng 梁静 尚永丰 | 2018 | 科学新闻2018，0，4： | 0 |
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