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| 1 | Erianin,a novel dibenzyl compound in Dendrobium extract,inhibits lung cancer cell growth and migration via calcium/calmodulin-dependent ferroptosis显示文摘Ferroptosis,a novel form of programmed cell death,is characterized by iron-dependent lipid peroxidation and has been shown to be involved in multiple diseases,including cancer.Stimulating ferroptosis in cancer cells may be a potential strategy for cancer therapy.Therefore,ferroptosis-inducing drugs are attracting more attention for cancer treatment.Here,we showed that erianin,a natural product isolated from Dendrobium chrysotoxum Lindl,exerted its anticancer activity by inducing cell death and inhibiting cell migration in lung cancer cells.Subsequently,we demonstrated for the first time that erianin induced ferroptotic cell death in lung cancer cells,which was accompanied by ROS accumulation,lipid peroxidation,and GSH depletion.The ferroptosis inhibitors Fer-1 and Lip-1 but not Z-VAD-FMK,CQ,or necrostatin-1 rescued erianin-induced cell death,indicating that ferroptosis contributed to erianin-induced cell death.Furthermore,we demonstrated that Ca^(2+)/CaM signaling was a critical mediator of erianin-induced ferroptosis and that blockade of this signaling significantly rescued cell death induced by erianin treatment by suppressing ferroptosis.Taken together,our data suggest that the natural product erianin exerts its anticancer effects by inducing Ca^(2+)/CaMdependent ferroptosis and inhibiting cell migration,and erianin will hopefully serve as a prospective compound for lung cancer treatment. | Peng Chen Qibiao Wu Jiao Feng Lili Yan Yitian Sun Shuiping Liu Yu Xiang Mingming Zhang Ting Pan Xiaying Chen Ting Duan Lijuan Zhai Bingtao Zhai Wengang Wang Ruonan Zhang Bi Chen Xuemeng Han Yicong Li Liuxi Chen Ying Liu Xingxing Huang Ting Jin Wenzheng Zhang Hong Luo Xiaohui Chen Yongqiang Li Qiujie Li Guohua Li Qin Zhang Lvjia Zhuo Zuyi Yang Huifen Tang Tian Xie Xiaoping Ouyang Xinbing Sui | 2020 | Signal Transduction and Targeted Therapy2020，5，1： | 42 |
| 2 | A novel m6A reader Prrc2a controls oligodendroglial specification and myelination显示文摘While N6-methyladenosine (m6A), the most abundant internal modification in eukaryotic mRNA, is linked to cell differentiation and tissue development, the biological significance of m6A modification in mammalian glial development remains unknown. Here, we identify a novel m6A reader, Prrc2a (Proline rich coiled-coil 2A), which controls oligodendrocyte specification and myelination. Nestin-Cre-mediated knockout of Prrc2a induces significant hypomyelination, decreased lifespan, as well as locomotive and cognitive defects in a mouse model. Further analyses reveal that Prrc2a is involved in oligodendrocyte progenitor cells (OPCs) proliferation and oligodendrocyte fate determination. Accordingly, oligodendroglial-lineage specific deletion of Prrc2a causes a similar phenotype of Nestin-Cre-mediated deletion. Combining transcriptome-wide RNA-seq, m6A-RIP-seq and Prrc2a RIP-seq analysis, we find that Olig2 is a critical downstream target gene of Prrc2a in oligodendrocyte development. Furthermore, Prrc2a stabilizes Olig2 mRNA through binding to a consensus GGACU motif in the Olig2 CDS (coding sequence) in an m6A-dependent manner. Interestingly, we also find that the m6A demethylase, Fto, erases the m6A modification of Olig2 mRNA and promotes its degradation. Together, our results indicate that Prrc2a plays an important role in oligodendrocyte specification through functioning as a novel m6A reader. These findings suggest a new avenue for the development of therapeutic strategies for hypomyelination-related neurological diseases. | Rong Wu Ang Li Baofa Sun Jian-Guang Sun Jinhua Zhang Ting Zhang Yusheng Chen Yujie Xiao Yuhao Gao Qingyang Zhang Jun Ma Xin Yang Yajin Liao Wei-Yi Lai Xiaolong Qi Shukun Wang Yousheng Shu Hai-Lin Wang Fengchao Wang Yun-Gui Yang Zengqiang Yuan | 2019 | Cell Research2019，29，1： | 32 |
| 3 | Analyses of hot and humid weather in Beijing city in summer and its dynamical identification显示文摘The circulation, hygrothermal property and moisture transport character of typical hot and humid weather were analyzed in Beijing areas from July 30 to August 4, 2002. It was pointed out that, under the control of subtropical anticyclone which stretches to the west and north, downdraft suppresses the lifting of lower-troposphere moisture, which makes moisture keep in the lower troposphere. That is the direct reason causing hot and humid weather. Considering the non-uniformity saturated character in real atmosphere, generalized moist potential vorticity (GMPV) equation is derived by the introduction of generalized moist potential temperature concept. The analysis of GMPV shows that negative GMPV anomaly occurs in the lower troposphere. It has indicative sense to hot and humid weather. Thus, the GMPV anomaly can be utilized to identify this kind of weather and to make a short-term prediction. | GAO Shouting ZHOU Yushu LEI Ting SUN Jianhua | 2005 | Science China Earth Sciences2005，48，z2： | 30 |
| 4 | Efficacy and safety of a novel anti-HER2 therapeutic antibody RC48 in patients with HER2-overexpressing,locally advanced or metastatic gastric or gastroesophageal junction cancer:a single-arm phase II study显示文摘Background:Current treatment options for human epidermal growth factor receptor 2(HER2)-overexpressing gastric cancer at third-line have shown limited clinical benefit.Further,there is no specific treatment for HER2 immunohistochemistry(IHC)2+and fluorescence in-situ hybridization-negative patients.Here,we report the efficacy and safety of a novel anti-HER2 antibody RC48 for patients with HER2-overexpressing,advanced gastric or gastroesophageal junction cancer.Methods:Patients with HER2-overexpressing(IHC 2+or 3+),locally advanced or metastatic gastric or gastroesophageal junction cancer who were under at least second-line therapy were eligible and received RC482.5 mg/kg alone every 2 weeks.The primary endpoint was the objective response rate(ORR)assessed by an independent review committee.Secondary endpoints included progressionfree survival(PFS),overall survival(OS),duration of response,time to progression,disease control rate,and safety.Results:Of 179 patients screened,125 were eligible and received RC48 treatment.The ORR was 24.8%(95%confidence interval[CI]:17.5%-33.3%).The median PFS and OS were 4.1 months(95%CI:3.7-4.9 months)and 7.9 months(95%CI:6.7-9.9 months),respectively.The most frequently reported adverse events were decreased white blood cell count(53.6%),asthenia(53.6%),hair loss(53.6%),decreased neutrophil count(52.0%),anemia(49.6%),and increased aspartate aminotransferase level(43.2%).Serious adverse events(SAEs)occurred in 45(36.0%)patients,and RC48-related SAEs were mainly decreased neutrophil count(3.2%).Seven patients had adverse events that led to death were not RC48-related.Conclusions:RC48 showed promising activity with manageable safety,suggesting potential application in patients with HER2-overexpressing,advanced gastric or gastroesophageal junction cancer who have previously received at least two lines of chemotherapy. | Zhi Peng Tianshu Liu Jia Wei Airong Wang Yifu He Liuzhong Yang Xizhi Zhang Nanfeng Fan Suxia Luo Zhen Li Kangsheng Gu Jianwei Lu Jianming Xu Qingxia Fan Ruihua Xu Liangming Zhang Enxiao Li Yuping Sun Guohua Yu Chunmei Bai Yong Liu Jiangzheng Zeng Jieer Ying Xinjun Liang Nong Xu Chao Gao Yongqian Shu Dong Ma Guanghai Dai Shengmian Li Ting Deng Yuehong Cui Jianmin Fang Yi Ba Lin Shen | 2021 | Cancer Communications2021，41，11： | 29 |
| 5 | Engineering application of membrane bioreactor for wastewater treatment in China: Current state and future prospect显示文摘中国是大规模膜生物反应器(MBR ) 的 forerunner 申请。自从第一大规模 MBR (10 000 m < 啜 class= “ a-plus-plus ” > 3 湩朠潯 ? 慦瑩? | Kang XIAO Ying XU Shuai LIANG Ting LEI Jianyu SUN Xianghua WEN Hongxun ZHANG Chunsheng CHEN Xia HUANG | 2014 | Frontiers of Environmental Science & Engineering2014，8，6： | 26 |
| 6 | Bone marrow mesenchymal stem cell therapy in ischemic stroke: mechanisms of action and treatment optimization strategies显示文摘Animal and clinical studies have confirmed the therapeutic effect of bone marrow mesenchymal stem cells on cerebral ischemia, but their mechanisms of action remain poorly understood. Here, we summarize the transplantation approaches, directional migration, differentiation, replacement, neural circuit reconstruction,angiogenesis, neurotrophic factor secretion, apoptosis, immunomodulation, multiple mechanisms of action,and optimization strategies for bone marrow mesenchymal stem cells in the treatment of ischemic stroke.We also explore the safety of bone marrow mesenchymal stem cell transplantation and conclude that bone marrow mesenchymal stem cell transplantation is an important direction for future treatment of cerebral ischemia. Determining the optimal timing and dose for the transplantation are important directions for future research. | Guihong Li Fengbo Yu Ting Lei Haijun Gao Peiwen Li Yuxue Sun Haiyan Huang Qingchun Mu | 2016 | Neural Regeneration Research2016，11，6： | 22 |
| 7 | Baicalin induces ferroptosis in bladder cancer cells by downregulating FTH1显示文摘Ferroptosis is a non-apoptotic regulated cell death caused by iron accumulation and subsequent lipid peroxidation.Currently,the therapeutic role of ferroptosis on cancer is gaining increasing interest.Baicalin an active component in Scutellaria baicalensis Georgi with anticancer potential various cancer types;however,the effects of baicalein on bladder cancer and the underlying molecular mechanisms remain largely unknown.In the study,we investigated the effect of baicalin on bladder cancer cells5637 and KU-19-19.As a result,we show baicalin exerted its anticancer activity by inducing apoptosis and cell death in bladder cancer cells.Subsequently,we for the first time demonstrate baicalin-induced ferroptotic cell death in vitro and in vivo,accompanied by reactive oxygen species(ROS) accumulation and intracellular chelate iron enrichment.The ferroptosis inhibitor deferoxamine but not necrostatin-1,chloroquine(CQ),N-acetyl-L-cysteine,L-glutathione reduced,or carbobenzoxy-valyl-alanyl-aspartyl-[O-methyl]-fluoromethylketone(Z-VAD-FMK) rescued baicalin-induced cell death,indicating ferroptosis contributed to baicalin-induced cell death.Mechanistically,we show that ferritin heavy chain1(FTH1) was a key determinant for baicalin-induced ferroptosis.Overexpression of FTH1 abrogated the anticancer effects of baicalin in both 5637 and KU19-19 cells.Taken together,our data for the first time suggest that the natural product baicalin exerts its anticancer activity by inducing FTH1-dependent ferroptosis,which will hopefully provide a prospective compound for bladder cancer treatment. | Na Kong Xiaying Chen Jiao Feng Ting Duan Shuiping Liu Xueni Sun Peng Chen Ting Pan Lili Yan Ting Jin Yu Xiang Quan Gao Chengyong Wen Weirui Ma Wencheng Liu Mingming Zhang Zuyi Yang Wengang Wang Ruonan Zhang Bi Chen Tian Xie Xinbing Sui Wei Tao | 2021 | Acta Pharmaceutica Sinica B2021，11，12： | 23 |
| 8 | A Pilot Study of the Therapeutic Efficacy and Mechanism of Artesunate in the MRL/lpr Murine Model of Systemic Lupus Erythematosus显示文摘Recent evidence indicates that artesunate has immunomodulatory properties that might be useful for treating autoimmune disease.In this study,we conducted a pilot study and explored the effect and mechanism of artesunate on the treatment of systemic lupus erythematosus using an MRL/lpr murine model.MRL/lpr mice were divided into control,cyclophosphamide(CTX)and artesunate treatment groups.Blood was collected to measure serum levels of creatinine,antinuclear antibody(ANA)and anti-double-stranded DNA(anti-dsDNA)antibody.Twenty-four-hour urine was collected to measure levels of proteinuria.The concentration of monocyte chemotactic protein-1(MCP-1)in serum and urine was measured.The expression of MCP-1 in kidney was detected by Western blot and immunohistochemistry assay,respectively.The expression of B cell activating factor(BAFF)in spleen was determined by real time-PCR and immunoblotting.We found that artesunate significantly increased the survival rate,body weight and blood leukocyte counts,and reduced the serum levels of ANA and anti-dsDNA antibody titer,24 h urinary protein,and serum creatinine.Our results indicated that artesunate could decrease MCP-1,major pro-inflammation cytokine,in serum,urine and kidney.We also found that the level of BAFF,the major B cell activation factor,was decreased in artesunate treated MRL/lpr mice.Its efficacy was comparable with that of CTX in this study.Taken together,we have demonstrated that artesunate can inhibit the progression of disease and reverse the pathologic lesion of lupus nephritis. | Ouyang Jin Huayong Zhang Zhifeng Gu Shengnan Zhao Ting Xu Kangxing Zhou Bo Jiang Jie Wang Xiaofeng Zeng Lingyun Sun | 2009 | Cellular & Molecular Immunology2009，6，6： | 20 |
| 9 | Whole-genome sequencing of 508 patients identifies key molecular features associated with poor prognosis in esophageal squamous cell carcinoma显示文摘Esophageal squamous cell carcinoma(ESCC)is a poor-prognosis cancer type with limited understanding of its molecular etiology.Using 508 ESCC genomes,we identified five novel significantly mutated genes and uncovered mutational signature clusters associated with metastasis and patients’outcomes.Several functional assays implicated that NFE2L2 may act as a tumor suppressor in ESCC and that mutations in NFE2L2 probably impaired its tumor-suppressive function,or even conferred oncogenic activities.Additionally,we found that the NFE2L2 mutations were significantly associated with worse prognosis of ESCC.We also identified potential noncoding driver mutations including hotspot mutations in the promoter region of SLC35E2 that were correlated with worse survival.Approximately 5.9%and 15.2%of patients had high tumor mutation burden or actionable mutations,respectively,and may benefit from immunotherapy or targeted therapies.We found clinically relevant coding and noncoding genomic alterations and revealed three major subtypes that robustly predicted patients’outcomes.Collectively,we report the largest dataset of genomic profiling of ESCC useful for developing ESCC-specific biomarkers for diagnosis and treatment. | Yongping Cui Hongyan Chen Ruibin Xi Heyang Cui Yahui Zhao Enwei Xu Ting Yan Xiaomei Lu Furong Huang Pengzhou Kong Yang Li Xiaolin Zhu Jiawei Wang Wenjie Zhu Jie Wang Yanchun Ma Yong Zhou Shiping Guo Ling Zhang Yiqian Liu Bin Wang Yanfeng Xi Ruifang Sun Xiao Yu Yuanfang Zhai Fang Wang Jian Yang Bin Yang Caixia Cheng Jing Liu Bin Song Hongyi Li Yi Wang Yingchun Zhang Xiaolong Cheng Qimin Zhan Yanhong Li Zhihua Liu-Show | 2020 | Cell Research2020，30，10： | 19 |
| 10 | p53 upregulated by HIF-la promotes hypoxiainduced G2/M arrest and renal fibrosis in vitro and in vivo显示文摘Hypoxia plays an important role in the genesis and progression of renal fibrosis.The underlying mechanisms, however, have not been sufficiently elucidated. We examined the role of p53 in hypoxia-induced renal fibrosis in cell culture (human and rat renal tubular epithelial cells) and a mouse unilateral ureteral obstruction (UUO) model. Cell cycle of tubular cells was determined by flow cytometry, and the expression of profibrogenic factors was determined by RT-PCR, immunohistochemistry, and western blotting. Chromatin immunoprecipitation and luciferase reporter experiments were performed to explore the effect of HIF-lα on p53 expression. We showed that, in hypoxic tubular cells, p53 upregulation suppressed the expression of CDK1 and cyclins Bl and DI, leading to cell cycle (G2/M) arrest (or delay) and higher expression of TGF-β, CTGF, collagens, and fibronectin. p53 suppression by siRNA or by a specific p53 inhibitor (PIF-α) triggered opposite effects preventing the G2/M arrest and profibrotic changes. In vivo experiments in the UUO model revealed similar antifibrotic results following intraperitoneal administration of PIF-α(2.2 mg/kg). Using gain-of-function, loss-of-function, and luciferase assays, we further identified an HRE3 region on the p53 promoter as the HIF-lα-binding site. The HIF-la-HRE3 binding resulted in a sharp transcriptional activation of p53. Collectively, we show the presence of a hypoxia-activated, p53-responsive profibrogenic pathway in the kidney. During hypoxia, p53 upregulation induced by HIF-la suppresses cell cycle progression, leading to the accumulation of G2/M cells, and activates profibrotic TGF-β and CTGF-mediated signaling pathways, causing extracellular matrix production and renal fibrosis. | Limin Liu Peng Zhang Ming Bai Lijie He Lei Zhang Ting Liu Zhen Yang Menglu Duan Minna Liu Baojian Liu Rui Du Qi Qian Shiren Sun | 2019 | Journal of Molecular Cell Biology2019，11，5： | 18 |
| 11 | Dynamic methylome of internal mRNA N^7-methylguanosine and its regulatory role in translation显示文摘Over 150 types of RNA modifications are identified in RNA molecules.Transcriptome profiling is one of the key steps in decoding the epitranscriptomic panorama of these chemical modifications and their potential functions.N7-methylguanosine(m7G)is one of the most abundant modifications present in tRNA,rRNA and mRNA 5’cap,and has critical roles in regulating RNA processing,metabolism and function.Besides its presence at the cap position in mRNAs,m7G is also identified in internal mRNA regions.However,its transcriptome-wide distribution and dynamic regulation within internal mRNA regions remain unknown.Here,we have established m7G individual-nucleotide-resolution cross-linking and immunoprecipitation with sequencing(m7G miCLIP-seq)to specifically detect internal mRNA m7G modification.Using this approach,we revealed that m7G is enriched at the 5’UTR region and AG-rich contexts,a feature that is well-conserved across different human/mouse cell lines and mouse tissues.Strikingly,the internal m7G modification is dynamically regulated under both H2O2 and heat shock treatments,with remarkable accumulations in the CDS and 3’UTR regions,and functions in promoting mRNA translation efficiency.Consistently,a PCAW 3’UTR minigene reporter harboring the native m7G modification site displays both enriched m7G modification and increased mRNA translation upon H2O2 treatment compared to the m7G site-mutated minigene reporter(G to A).Taken together,our findings unravel the dynamic profiles of internal mRNA m7G methylome and highlight m7G as a novel epitranscriptomic marker with regulatory roles in translation. | Lionel Malbec Ting Zhang Yu-Sheng Chen Ying Zhang Bao-Fa Sun Bo-Yang Shi Yong-Liang Zhao Ying Yang Yun-Gui Yang | 2019 | Cell Research2019，29，11： | 17 |
| 12 | Etoricoxib versus indometacin in the treatment of Chinese patients with acute gouty arthritis: a randomized double-blind trial显示文摘 | LI Ting CHEN Shun-le DAI Qing HAN Xing-hai LI Zhan-guo WU Dong-hai ZHANG Xiao GU Jie-ruo YANGNan-ping SUN Ling-yun ZHANG Miu-jia LI Xing-fu and BAO Chun-de | 2013 | Chinese Medical Journal2013，，10： | 17 |
| 13 | An HBV-encoded miRNA activates innate immunity to restrict HBV replication显示文摘We previously identified that hepatitis B virus(HBV)encodes a microRNA(HBV-miR-3)that restrains HBV replication by targeting the HBV transcript.However,whether HBV-miR-3 affects host innate immunity to modulate HBV replication remains unclear.Here,we examined the vital functions of HBV-miR-3 in the innate immune response after HBV infection.We found that HBV-miR-3 expression gradually increased in a dose-and time-dependent manner in HBV-infected HepG2-NTCP cells.HBV-miR-3 activated the JAK/STAT signaling pathway by downregulating SOCS5 in hepatocytes,thereby enhancing the IFN-induced anti-HBV effect.In addition,HBVmiR-3 in exosomes facilitated the Ml polarization of macrophages.Furthermore,exosomes containing HBV-miR-3 enhanced the secretion of IL-6 via inhibiting the SOCS5-mediated ubiquitination of EGFR.In short,these results demonstrate that HBV-miR-3 activates the innate immune response to restrain HBV replication by multiple pathways,which may suppress HBV-induced acute liver cell injury and affect the progression of persistent HBV infection. | Xiaoqing Zhao Lu Sun Ting Mu Jianying Yi Chaoqun Ma Hong Xie Min Liu Hua Tang | 2020 | Journal of Molecular Cell Biology2020，12，4： | 17 |
| 14 | Progress of the key materials for organic solar cells显示文摘Organic solar cells have attracted academic and industrial interests due to the advantages like lightweight,flexibility and roll-to-roll fabrication.Nowadays,18%power conversion efficiency has been achieved in the state-of-the-art organic solar cells.The recent rapid progress in organic solar cells relies on the continuously emerging new materials and device fabrication technologies,and the deep understanding on film morphology,molecular packing and device physics.Donor and acceptor materials are the key materials for organic solar cells since they determine the device performance.The past 25 years have witnessed an odyssey in developing high-performance donors and acceptors.In this review,we focus on those star materials and milestone work,and introduce the molecular structure evolution of key materials.These key materials include homopolymer donors,D-A copolymer donors,A-D-A small molecular donors,fullerene acceptors and nonfullerene acceptors.At last,we outlook the challenges and very important directions in key materials development. | Yang Tong Zuo Xiao Xiaoyan Du Chuantian Zuo Yuelong Li Menglan Lv Yongbo Yuan Chenyi Yi Feng Hao Yong Hua Ting Lei Qianqian Lin Kuan Sun Dewei Zhao Chunhui Duan Xiangfeng Shao Wei Li Hin-Lap Yip Zhengguo Xiaol Bin Zhang Qingzhen Bian Yuanhang Cheng Shengjian Liu Ming Cheng Zhiwen Jin Shangfeng Yang Liming Ding | 2020 | Science China Chemistry2020，63，6： | 15 |
| 15 | Transgenic rhesus monkeys carrying the human MCPH1 gene copies show human-like neoteny of brain development显示文摘Brain size and cognitive skills are the most dramatically changed traits in humans during evolution and yet the genetic mechanisms underlying these human-specific changes remain elusive.Here,we successfully generated 11 transgenic rhesus monkeys(8 first-generation and 3 second-generation)carrying human copies of MCPH1,an important gene for brain development and brain evolution.Brain-image and tissue-section analyses indicated an altered pattern of neural-cell differentiation,resulting in a delayed neuronal maturation and neural-fiber myelination of the transgenic monkeys,similar to the known evolutionary change of developmental delay(neoteny)in humans.Further brain-transcriptome and tissue-section analyses of major developmental stages showed a marked human-like expression delay of neuron differentiation and synaptic-signaling genes,providing a molecular explanation for the observed brain-developmental delay of the transgenic monkeys.More importantly,the transgenic monkeys exhibited better short-term memory and shorter reaction time compared with the wild-type controls in the delayed-matching-to-sample task.The presented data represent the first attempt to experimentally interrogate the genetic basis of human brain origin using a transgenic monkey model and it values the use of non-human primates in understanding unique human traits. | Lei Shi Xin Luo Jin Jiang Yongchang chen Cirong Liu Ting Hu Min Li Qiang Lin Yanjiao Li Jun Huang Hong Wang Yuyu Niu Yundi Shi Martin Styner Jianhong Wang Yi Lu Xuejin Sun Hualin Yu Weizhi Ji Bing Su | 2019 | National Science Review2019，6，3： | 12 |
| 16 | Characteristics of Proinflammatory Cytokines and Chemokines in Airways of Asthmatics: Relationships with Disease Severity and Infiltration of Inflammatory Cells显示文摘 | Ting Yang Yan Li Zhe Lyu Kewu Huang Chris J Corrigan Sun Ying Wei Wang Chen Wang | 2017 | Chinese Medical Journal2017，，17： | 12 |
| 17 | Alfalfa-containing diets alter luminal microbiota structure and short chain fatty acid sensing in the caecal mucosa of pigs显示文摘Background: Pork produced by outdoor-reared pigs raised mostly on alfalfa pastures attracts increasing population of consumer from most of the world. In China, pigs were raised with alfalfa-containing diets to seek for good quality pork.However, the influence of dietary alfalfa involving high level of insoluble dietary fiber(IDF) on pig intestinal luminal microbiota composition remains unclear. The objective of this study was to investigate the effects of alfalfa on luminal microbiota and short chain fatty acids(SCFA) production, and gene expressions involved in SCFA sensing, transporting and absorbing in pig caecal mucosa.Results: Twenty-four growing pigs were randomly allotted to four diets containing 0%, 5%, 10% and 15% alfalfa meal for a 28-d experiment. Ingestion of alfalfa meal-contained diets significantly increased the ratio of body weight gain to feed consumption. Illumina MiS eq sequencing of the V3 region of the 16 S r RNA genes showed that alfalfa-containing diet significantly decreased the relative abundance of genera Turicibacter, Acidiphilium, Paracoccus, Propionibacterium,Corynebacterium, Pseudomonas, Acinetobacter, and Staphylococcus, and increased the relative abundance of genera Lachnospira, Marvinbryantia, and Desulfovibrio in the caecal digesta. Butyrate concentration was significantly increased in the hindgut by the supplementation of alfalfa meal in diets. The m RNA gene expressions of FFAR3, SMCT1, MCT1,PYY, and GCG were significantly increased in the caecal mucosa of pigs fed alfalfa meal.Conclusions: Our results suggested that alfalfa-containing diet has exerted significant impacts on caecal microbiota composition, butyrate concentration and significantly upregulated m RNA expression of host caecal mucosal genes involved in SCFA sensing and absorption as well as regulation of satiety. | Jiawei Wang Chunfu Qin Ting He Kai Qiu Wenjuan Sun Xin Zhang Ning Jiao Weiyun Zhu Jingdong Yin | 2018 | Journal of Animal Science and Biotechnology2018，9，2： | 12 |
| 18 | Intrinsic apoptotic pathway and G2/M cell cycle arrest involved in tubeimoside I-induced EC109 cell death显示文摘Objective: Squamous esophageal carcinoma is highly prevalent in developing countries, especially in China. Tu Bei Mu (TBM), a traditional folk medicine, has been used to treat esophageal squamous cell carcinoma (ESCC) for a long term. tubeimoside I (TBMS1) is the main component of TBM, exhibiting great anticancer potential. In this study, we investigated the mechanism of TBMS1 cytotoxic effect on EC109 cells. Methods: Comparative nuclear proteomic approach was applied in the current study and we identified several altered protein spots. Further biochemical studies were carried out to detect the mitochondrial membrane potential, cell cycle and corresponding proteins' expression and location. Results: Subcellular proteomic study in the nucleus from EC109 cells revealed that altered proteins were associated with mitochondrial function and cell proliferation. Further biochemical studies showed that TBMS1-induced molecular events were related to mitochondria-induced intrinsic apoptosis and P21-cyclin B1/cdc2 complex-related G2/M cell cycle arrest. Conclusions: Considering the conventional application of TBM in esophageal cancer, TBMS1 therefore may have a great potential as a chemotherapeutic drug candidate for ESCC. | Yang Xu Guanghui Wang Quancheng Chen Ting Lin Zhiping Zeng Qiang Luo Jie Liu Cuiling Sun | 2013 | Chinese Journal of Cancer Research2013，25，3： | 12 |
| 19 | Jianpijiedu Fang improves survival of hepatocarcinoma mice by affecting phosphatase and tensin homolog, phosphoinositide 3-kinase, and focal adhesion kinase显示文摘OBJECTIVE: To investigate the effect of Jianpijiedu Fang (JPJDF) on phosphatase and tensin homolog (PTEN), phosphoinositide 3-kinase (PI3K), and focal adhesion kinase (FAK), and on the survival of hepatocellular carcinoma (HCC) nude mice. METHODS: Forty male nude mice were randomly divided into 4 groups. Human HCC tissue was implanted in the livers of three groups. After 24 h, the three groups were treated respectively with JPJDF (37.5 g/kg), saline (20 mL/kg) and Tegafur (FT-207, 160 mg/kg) once a day for 10 weeks. The control group without implanting the tissue was concurrently treated with saline (20 mL/kg). The survival data and body weight of all mice were recorded, and expression levels of PTEN, PI3K and FAK in normal tissue and cancer tissue of the livers were eval-uated with immunohistochemical method. RESULTS: The cumulative survival rate of the mice in the JPJDF group was higher than those of the other groups. The rate of weight loss was the lowest in JPJDF group. The survivability and weight loss rate in FT-207 group were the poorest in all groups. The expression intensity of PTEN was higher in normal tissues than in cancer tissues, and lower in the normal tissues of HCC models than in that of mice without HCC. The PTEN expression intensity in normal tissue and cancer tissue from mice treated with FT-207 were lower than that from the mice treated with JPJDF or saline.The expression intensity of PI3K was higher in cancer tissue than in normal tissue. The PI3K expression intensity was the lowest in normal tissue and cancer tissue from mice treated with JPJDF, and the intensity from mice treated with FT-207 was the highest. In mice treated with JPJDF, the expression intensity of FAK was higher in the normal tissue and lower in the cancer tissue than those of the other treatment groups. CONCLUSION: The mechanism accounting for the prolonged survival of HCC-bearing mice treated with JPJDF might be related to the reduction in weight loss and the benign regulation of PTEN, PI3K, and FAK. | Baoguo Sun Jun Meng Ting Xiang Zexiong Chen Yulong Li Lisha Lu Shijun Zhang Xiaolin Chen | 2013 | Journal of Traditional Chinese Medicine2013，33，4： | 12 |
| 20 | NF-κB signaling in inflammation显示文摘The transcription factor NF-κB regulates multiple aspects of innate and adaptive immune functions and serves as a pivotal mediator of inflammatory responses.NF-κB induces the expression of various pro-inflammatory genes,including those encoding cytokines and chemokines,and also participates in inflammasome regulation.In addition,NF-κB plays a critical role in regulating the survival,activation and differentiation of innate immune cells and inflammatory T cells.Consequently,deregulated NF-κB activation contributes to the pathogenic processes of various inflammatory diseases.In this review,we will discuss the activation and function of NF-κB in association with inflammatory diseases and highlight the development of therapeutic strategies based on NF-κB inhibition. | Ting Liu Lingyun Zhang Donghyun Joo Shao-Cong Sun | 2017 | Signal Transduction and Targeted Therapy2017，2，1： | 12 |
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