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LSM12 facilitates the progression of colorectal cancer by activating the WNT/CTNNB1 signaling pathway

Oncology Research 2022年第6期30卷 289-300页

作者： YAN ZHUANG CHUNLAN NING PENGFEI LIU YANPENG ZHAO YUE LI ZHENCHI MA LULING SHAN YINGZHE PIAO PENG ZHAO XUN JIN Department of Colorectal Oncology Tianjin Medical University Cancer Institute&HospitalNational Clinical Research Center for CancerTianjin’s Clinical Research Center for CancerKey Laboratory of Cancer Prevention and TherapyTianjin300060China Department of Biochemistry and Molecular Biology Tianjin Medical University Cancer Institute and HospitalNational Clinical Research Center for CancerTianjin’s Clinical Research Center for CancerKey Laboratory of Cancer Prevention and TherapyTianjin300060China Tianjin Medical University Tianjin300070China Department of Oncology Tianjin Academy of Traditional Chinese Medicine Affiliated HospitalTianjin300120China Tianjin Marvel Medical Laboratory Tianjin Marvelbio Technology Co.Ltd.Tianjin300381China Department of Gastro Colorectal Oncology Tianjin Cancer Hospital Airport HospitalTianjin300304China Department of Neuro-Oncology and Neurosurgery Tianjin Medical University Cancer Institute&HospitalNational Clinical Research Center for CancerKey Laboratory of Cancer Prevention and Therapy TianjinTianjin’s Clinical Research Center for CancerTianjin300060China

Aberrant activation of the WNT signaling pathway is a joint event in colorectal cancer(CRC),but the molecular mechanism is still ***,RNA-splicing factor LSM12(like-Sm protein 12)is highly expressed in CRC *** study aimed to verify whether LSM12 is involved in regulating CRC progression via regulating the WNT signaling ***,we found that LSM12 is highly expressed in CRC patient-derived tissues and ***12 is involved in the proliferation,invasion,and apoptosis of CRC cells,similar to the function of WNT signaling in ***,protein interaction simulation and biochemical experiments proved that LSM12 directly binds to CTNNB1(also known asβ-Catenin)and regulates its protein stability to affect the CTTNB1-LEF1-TCF1 transcriptional complex formation and the associated WNT downstream signaling ***12 depletion in CRC cells decreased the in vivo tumor growth through repression of cancer cell growth and acceleration of cancer cell *** together,we suggest that the high expression of LSM12 is a novel factor leading to aberrant WNT signaling activation,and that strategies targeting this molecular mechanism may contribute to developing a new therapeutic method for CRC.

关键词： CRC LSM12 WNT CTNNB1 apotosis

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Regulation of innate immune responses by rabies virus

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Animal Models and Experimental Medicine 2022年第5期5卷 418-429页

作者： Haili Zhang Jingbo Huang Yumeng Song Xingqi Liu Meichen Qian Pei Huang Yuanyuan Li Ling Zhao Hualei Wang State Key Laboratory for Zoonotic Diseases Key Laboratory for Zoonosis Research of the Ministry of EducationInstitute of Zoonosisand College of Veterinary MedicineJilin UniversityChangchunChina State Key Laboratory of Agricultural Microbiology Huazhong Agricultural UniversityWuhanChina

Rabies virus(RABV)is an infectious and neurotropic pathogen that causes rabies and infects humans and almost all warm-blooded animals,posing a great threat to people and public *** is well known that innate immunity is the critical first line of host defense against viral *** monitors the invading pathogens by recognizing the pathogen-associated molecular patterns and danger-associated molecular patterns through pattern-recognition receptors,leading to the production of type I interferons(IFNα/β),inflammatory cytokines,and chemokines,or the activation of autophagy or apoptosis to inhibit virus *** the case of RABV,the innate immune response is usually triggered when the skin or muscle is bitten or ***,RABV has evolved many ways to escape or even hijack innate immune response to complete its own replication and eventually invades the central nervous system(CNS).Once RABV reaches the CNS,it cannot be wiped out by the immune system or any ***,a better understanding of the interplay between RABV and innate immu-nity is necessary to develop effective strategies to combat its ***,we review the innate immune responses induced by RABV and illustrate the antagonism mechanisms of RABV to provide new insights for the control of rabies.

关键词： apotosis autophagy infectious disease and host defense innate immunity and inflammation rabies virus

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Vascular endothelial growth inhibitor affects the invasion, apoptosis and vascularisation in breast cancer cell line MDA-MB-231

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Chinese Medical Journal 2014年第10期127卷 1947-1953页

作者： Gao Yinguang Ge Zhicheng Zhang Zhongtao Bai Zhigang Ma Xuemei Wang Yu Department of General Surgery Beijing Friendship Hospital CapitalMedical University Beijing 100050 China

Background Breast cancer is one of the most common malignant female diseases *** is a significant threat to every woman＇s *** endothelial growth inhibitor （VEGI） is known to be abundant in endothelial *** to previous literature,overexpression of VEGI has been shown to inhibit tumor neovascularisation and progression in cellular and animal models,but there has been limited research on the significance of VEGI in the breast *** In our study,cell lines MDA-MB-231 were first constructed in which VEGI mediated by lentivirus *** effects of VEGI over-expression on MDA-MB-231 cells were investigated both in vitro and in *** expression of VEGI in the MDA-MB-231 cells after infection of lentivirus was analyzed using real-time PCR and Western *** effect of the biological characteristics of MDA-MB-231 cells was assessed by growth,invasion,adhesion,and migration assay with subcutaneous tumor-bearing nude mice *** the growth curves of the subcutaneous tumors were *** of VEGI,CD31 and CD34 in the tumors were analyzed by immunohistochemistry and apoptosis was detected by flow cytometry and *** Infection of MDA-MB-231 cells within the lentivirus resulted in approximately a 1 000-fold increase in the expression of *** can be seen in the invasion,adhesion and migration assay,the over-expression of VEGI can inhibit the ability of MDA-MB-231 cells during migration,adhesion and *** volume of the subcutaneous tumor in the over-expression group was distinctly and significantly less than that of the control *** analysis of the tumor biopsies cleady showed the expression of VEGI in the over-expression group increased while CD31 and CD34 decreased *** vitro and in vivo,the early apoptosis rate and the apoptosis index were increased within the VEGI over-expression group as compared with the control *** Taken to

关键词： breast cancer lentivirus MDA-MB-231 apotosis

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Preparation, Release-control and Cell Apoptosis of C_6 Glioma Cells in PEG-PLGA-Rg3 Nanoparticles

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Chemical Research in Chinese Universities 2010年第5期26卷 780-784页

作者： BIE Li YUAN Hong-yan WANG Xin ZHAO Gang LIU Xing-ji Department of Neurosurgery First Clinical Hospital Department of Immunology Norman Bethune College of Medicine Jilin University Changchun 130021 P. R. China Center of Tumor Biotherapy Second Clinical Hospital Jilin University Changchun 130041 P. R. China

With biodegradable material poly（ethylene glycol）-poly（lactide-co-glycolide）（PEG-PLGA） as substrate, the size distribution of Rg3-NPs was approved by the scanning electron microscopy. MTT assay was used to detect the effects of Rg3-NPs on the growth rate of C6 cells at various concentrations and flow cytometry（FCM） was applied to assay the cell cycle and cell apoptosis of C6 glioma cells. Western blot analysis was used to measure the protein level of PCNA. The results show that Rg3-NPs are slick and uniformity, the average diameter of the nanoparticles is about 75-90 nm, entrapment efficiency is （89.7±1.7）%. MTT assay shows the growth of C6 Glioma Cells can be significantly inhibited by Rg3-NPs in a dose-dependence manner. FCM and Western blot analysis show Rg3 can be released from the conjugated nanoparticles to function in the cell nuclei so as to lead to the changes in the growth cycle of the cells, which results in the arrest of G0-G1 cell cycle and induces the apoptosis of C6 cells. Therefore, Rg3-NPs may be used for the auxiliary therapy of brain glioma.

关键词： Ginsenoside Rg3 Poly(D,L-lactide-co-glycolide) Characteristics of physical chemistry C6 glioma cell apotosis

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Specific regulator of eosinophil apoptosis： Siglec-8 new hope for bronchial asthma treatment

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Chinese Medical Journal 2012年第11期125卷 2048-2052页

作者： FENG Yin-he MAO Hui Department of Respiratory Medicine West China Hospital of Sichuan UniversityChengduSichuan 610041China

Objective It is known that Siglec-8 is selectively expressed on human eosinophils at a high level and mediates eosinophil apoptosis when crosslinked with its antibody. The aim of our review is to elucidate the molecular and biological characteristic of Siglec-8 and then discuss the function and possible mechanisms of Siglec-8 in eosinophils. Thereby, we will expand our understanding to the regulation of eosinophil apoptosis, and provide important clues to the treatment of asthma and other hyper-eosinophilic diseases. Data sources Most articles were identified by searching of PubMed online resources using the key term Siglecs. Study selection Mainly original milestone articles and critical reviews written by major pioneer investigators in the field were selected. Results Siglec-8 is selectively expressed on human eosinophil and can specifically induce eosinophil apoptosis. Conclusion The restricted expression of Siglec-8 on human eosinophil and the rapid progress in understanding its role as cell signaling and activation of death receptors have made it an attractive target for treatment of asthma and other hyper-eosinophilic diseases.

关键词： asthma, eosinophil apotosis Siglec-8

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Overexpression of Nurrl Enhances the Vulnerability of SK-N-SH Cells to Neurotoxin 6-OHDA

Overexpression of Nurrl Enhances the Vulnerability of SK-N-S...

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中国细胞生物学学会第九次会员代表大会暨青年学术大会

作者： Yong-Mei Zhao~1 Yang Liu~1 Hai-Yan Zhang~2 Qun-Yuan Xu~3 1 Key Laboratory for Neurodegenerative Diseases of Ministry of Education,Xuanwu Hospital of Capital Medical University,Beijing 100053 2 Department of Cell Biology,Capital Medical University,Beijing 100069 3 Beijing Institute for Neuroscience,Capital Medical University,Beijing 100069,China

Objectives:To investigate whether overexpression of Nurr1(nuclear receptor-related factor 1)enhances the vulnerability of SK-N-SH ceils to neurotoxin ***1 is a transcription factor of the steriod/thyroxin hormone nucl... 详细信息

关键词： Nurrl overexpression 6-OHDA apotosis

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Prevention and mechanism of fibroblast apoptosis induced by ultraviolet

Prevention and mechanism of fibroblast apoptosis induced by ...

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International Forum 2003 Academic Conference of Dermatology of the Integration of TCM with Western Medicine

作者： Song Xiuzu, Xia Jiping, Bi Zhigang Department of Dermatology, The First Affiliated Hospital, Nanjing Medical University, Nanjing, 210029, China

Objective: To explore the mechanism of ultraviolet-induced fibroblastapoptosis and the protective effects of EGCG, a major green tea catechin,on the ultraviolet-induced apoptosis.

关键词： Ultraviolet apotosis Fibroblast Epigallocatechin-gallate

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The study on mechanism of anti- apoptotic function of 3β-hydroxysteroid-△24reductase(DHCR24) in the respect of its topological localization on endoplasmic membrane

The study on mechanism of anti- apoptotic function of 3β-hy...

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遗传学进步促进粮食安全与人口健康高峰论坛

作者： Li Yang,Liu Ting,Liu Zehui,Zhang Yong,Jia Dan,Chen Shuchao,Lu Xiuli Department of Biochemistry and Cell Biology of Life Science,Liaoning University,Shenyang 110036,China.

DHCR24 encodes 3-hydroxysteroid-△24 reductase,which converts desmosterol *** recent years,it is demonstrated that DHCR24 has the ability of anti-apoptotic induced by oxidative stress or endoplasmic reticulum(ER) stress as a Reactive oxygen Species(ROS) scavenger,for which it needs its FAD-binding *** previous studies showed that DHCR24 is an transmembrane protein which is mainly located on ER,but the membrane toplogy of DHCR24 on ER and the functional significance of its FAD-binding domain are not completely *** order to study its membrane topology and that whether its location on ER membrane affects its ROS scavenging function,we has successfully constructed three recombinant plasmids,which were N-terminally DsRed-tagged,C-terminally EGFP-tagged full-lenghth DHCR24 and N-terminally DsRed-tagged transmembrane(TM) deleted DHCR24,then transfected murine neuroblastoma cells(N2A),analyzed its membrane topology by fluorescent Protease Protection(FPP) and measured the intracellular ROS using H2DCFHDA after HO *** FPP assay demonstrated that the membrane topolofy of DHCR24 with an N-terminal luminal/C-terminal cytoplasmic *** of intracellular ROS revealed that the ROS levels of cells infected by plasmids driving expression of full-length DHCR24 or the TM deleted DHCR24 mutation were lower than those of control cells,suggesting that the ER membrane targeting of DHCR24 is not required for its enzymatic ROS scavenging *** is reported that DHCR24 can resist apoptosis by inhibiting the activation of caspase-3 as its *** this study,we found that caspase-3 is activated by the method of immumochemical fluorescence after HO exposure, suggersting the location of caspase 3-cleaving site facing cytoplasm is requered for its anti-apoptotic function.

关键词： DHCR24 membrane topology apotosis

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Adiponectin Inhibits Hepatocellular Carcinoma Through Redox Signalings

Adiponectin Inhibits Hepatocellular Carcinoma Through Redox ...

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第八届全国医学生物化学与分子生物学第五届全国临床应用生...

作者： Chen-Guang Zhang Ji-Fang Yuan Su-Qian Xing Hui-Min Yang Shu-Dong Zhao Hong Zhang Department of Medical Genetics Capital Medical University Deparrment of Neurobiology Key Laboratory for Neurodegenerative Disease of the Mini stry of EducationCapital Medical University School of Basic Medical Sciences Capital Medical University

Adiponec tin inhibits Hepatocellular Carcinoma(HCC),but the underlying mechanism remains *** results indicate that oxidative stress might play an important role in this *** of HCC cells with adiponectin decreased the cell viability accompa nied by an increase of intracellular reactive oxygen species(ROS) *** of anti-oxidant proteins or pretreatment with reductant N-acetyl cysteine(NAC)in HCC cells could attenuate or even reverse the inhibitory effect of *** further explore d the role of ROS in adiponection-induced apoptosis HCC and found that the increase of the intracellular ROS level increased the phosphorylation level of C-Jun-amino-terminal kinase(JNK) and cyctochrom c release from the mitochondria,as well as decreased ratio of Bax/Bcl2,activation of caspase3 and increased level of polyADP-ribosepolymerase(PARP)*** findings added new insight into the mechanism of HCC and probably provided a new therapeutic target for HCC.

关键词： adiponectin ROS HCC apotosis

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The effects of overexpression of Nurrl on SK-N-SH cells vulnerability to neurotoxin 6-OHDA

The effects of overexpression of Nurrl on SK-N-SH cells vuln...

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中国神经科学学会第四次会员代表大会暨第七届全国学术会议

作者： Yongmei ZHAO~1,Yang LIU~1,Haiyan ZHANG~2,Weihong LI~2,Qunyuan XU~3 1 Key Laboratory for Neurodegenerative Diseases of Ministry of Education,Xuanwu Hospital,Capital Medical University, Beijing 100053 2 Department of Cell Biology,Capital Medical University,Beijing 100069 3 Beijing Institute for Neuroscience,Capital Medical University,Beijing 100069

＜正＞Background Nurr1（nuclear receptor-related factor 1）,a transcription factor of the steriod/thyroxin hormone nuclear receptor superfamily,is highly expressed in mesencephalic dopamine（DA） *** is specifically required for the induction of ventral midbrain DArgic neurons and important for development and survival of mature DArgic neurons,the cells primarily lost in human Parkinson’s disease（PD）.In homozygous Nurr1-deficient mice,DArgic neurons fail to develop in the substantia nigra and ventrotegmental areas but are preserved in other brain *** observations suggest that Nurrl may play an important role in maintaining mature mesencephalic DArgic neuron function and may be one of the potential susceptibility factors for *** To investigate possible correlation between the expression of Nurrl gene and selective cell death of DArgic ***:a human neuroblastoma-derived cell line SK-N-SH which do not express endogenous Nurrl were transfected with the pBK-RSV-Nurr1 plasmid by LipofectAMINE and selected by ***-N-SH and SK-N-SH cells over-expressing Nurrlgene（SK-N-SH/Nurr1） were used as models to investigate the effects of overexpression of Nurrl on SK-N-SH cells vulnerability to neurotoxin ***（1） Nurr1 gene was highly overexpressed in transgenetic SK-N-SH/Nurr1 cells and cell proliferation in SK-N-SH/Nurr1 cells were *** Nurr1-overexpressing cells showed a significantly slow growth rate about（29.6±3.8）%decrease of that in SK-N-SH cells,which was might due to a marginal block in the G0/G1 to S phase transition,indicating Nurrl gene inhibited cell proliferation in SK-N-SH/ Nurrl cells.（2） The cell survival of Nurr1-overexpression SK-N-SH/Nurr1 cells was significantly inhibited by 6-OHDA,and the distribution of both cells at each phase in cell cycle were *** with 50μM6-OHDA changed SK-N-SH/Nurr1 cells morphology within 1 hr,accompanied by retraction of processes,shrinkage of cell body,whereas SK-N-SH c

关键词： Nurr1 Overexpression 6-OHDA apotosis

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