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The Zuo Jin Wan Formula increases chemosensitivity of human primary gastric cancer cells by AKT mediated mitochondrial translocation of cofilin-1

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Chinese Journal of Natural Medicines 2019年第3期17卷 198-208页

作者： SUN Meng-Yao WANG Dan-Dan SUN Jian ZHAO Xiao-Hua CAI Si WU Qiu-Xue JIE Tao NI Zhen-Hua SUN Jian-Yue TANG Qing-Feng Department of Clinical Laboratory and Central Laboratory Putuo Hospital Shanghai University of Traditional Chinese Medicine Institute of Interdisciplinary Medical Sciences Shanghai University of Traditional Chinese Medicine Department of Clinical Laboratory Shuguang Hospital Shanghai University of Traditional Chinese Medicine Department of Pediatrics Putuo Hospital Shanghai University of Traditional Chinese Medicine

Resistance to cisplatin(DDP)-based chemotherapy is a major cause of treatment failure in human gastric cancer(GC). It is necessary to identify the drugs to re-sensitize GC cells to DDP. In our previous research, Zuo Jin Wan Formula(ZJW) has been proved could increase the mitochondrial apoptosis via cofilin-1 in a immortalized cell line, SGC-7901/DDP. Due to the immortalized cells may still difficult highly recapitulate the important molecular events in vivo, primary GC cells model derived from clinical patient was constructed in the present study to further evaluate the effect of ZJW and the underlying molecular mechanism. Immunofluorescent staining was used to indentify primary cultured human GC cells. Western blotting was carried out to detect the protein expression. Cell Counting Kit-8(CCK-8) was used to evaluate cell proliferation. Flow cytometry analysis was performed to assess cell apoptosis. ZJW inhibited proliferation and induced apoptosis in primary DDP-resistant GC cells. Notably, the apoptosis in GC cells was mediated by inducing cofilin-1 mitochondrial translocation, down-regulating Bcl-2 and up-regulating Bax expression. Surprisingly, the level of p-AKT protein was higher in DDP-resistant GC cells than that of the DDP-sensitive GC cells, and the activation of AKT could attenuate ZJW-induced sensitivity to DDP. These data revealed that ZJW can increase the chemosensitivity in DDP-resistant primary GC cells by inducing mitochondrial apoptosis and AKT inactivation. The combining chemotherapy with ZJW may be an effective therapeutic strategy for GC chemoresistance patients.

关键词： Primary GC cells ZJW AKT chemoresistance

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Epithelial protein lost in neoplasm (EPLIN):Beyond a tumor suppressor

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Genes & Diseases 2017年第2期4卷 100-107页

作者： Daqing Wu Georgia Cancer Center and Department of Biochemistry and Molecular Biology Medical College of GeorgiaAugusta UniversityAugustaGAUSA MetCure Therapeutics LLC AtlantaGAUSA

The majority of cancer-related deaths are caused by tumor recurrence,metastasis and therapeutic resistance.During the late stages of tumor progression,multiple factors are involved,including the downregulation and/or loss of function of metastasis suppressors.Epithelial protein lost in neoplasm(EPLIN),an actin-binding protein,was initially identified as a putative tumor suppressor that is frequently downregulated in epithelial tumors.Recent evidence indicates that EPLIN may negatively regulate epithelia-to-mesenchymal transition(EMT),a crucial process by which cancer cells acquire invasive capabilities and therapeutic resistance.Importantly,downregulation of EPLIN is associated with clinical metastasis in a variety of solid tumors,suggesting that EPLIN could be a suppressor of metastasis.In this review,I will discuss the regulation and function of EPLIN in human cancer cells and explore the clinical significance of EPLIN in metastatic disease.

关键词： Actin cytoskeleton chemoresistance Epithelial-tomesenchymal transition EPLIN Metastasis suppressor Tumor suppressor

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Quantitative differences in protein expression between cisplatin sensitive COC1 ovarian carcinoma cells and cisplatin resistant COC1/DDP cells

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Chinese Medical Journal 2009年第7期122卷 865-869页

作者： WANG Hui-xiang SUN Wei LI He-lian ZHANG Wei-yuan Department of Obstetrics and Gynecology Second HospitalTsinghua University Beijing 100049 China Department of General Surgery Second Hospital China MedicalUniversity Shenyang Liaoning 110001 China Department of Obstetrics and Gynecology Second Hospital JilinUniversity Changchun Jilin 130041 China Department of Obstetrics and Gynecology Beijing Obstetrics andGynecology Hospital Capital Medical University Beijing 100026China

Ovarian cancer is the second most common cancer of the reproductive system in women and is the leading cause of death from gynecological cancers. Despite good response to surgery and initial chemotherapy, the resistance to platinum in some ovarian cancers represents a major obstacle to successful therapy. A number of mechanisms for ovarian cancer platinum resistance have been reported. These mechanisms include the reduction of cisplatin accumulation within cancer cells, the ability to detoxify cisplatin, faster repair of cisplatin-DNA adducts, modulation of apoptotic pathways, up-regulation of transcription factors, and a higher concentration of glutathione and metallothioneins.

关键词： chemoresistance ovarian cancer proteomics molecular markers gel electrophoresis

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Tumor cells educate mesenchymal stromal cells to release chemoprotective and immunomodulatory factors

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Journal of Molecular Cell Biology 2020年第3期12卷 202-215页

作者： Augustin Le Naour Melissa Prat Benolt Thibault Renaud Mével Léa Lemaitre Helene Leray Marie-Veronique Joubert Kimberley Coulson Muriel Golzio Lise Lefevre Eliane Mery Alejandra Martinez Gwénael Ferron Jean-Pierre Delord Agnès Coste Bettina Couderc Institut Claudius Regaud-IUCT Oncopole Universite de ToulouseToulouseFrance INSERM UMR 1037 Cancer Research Center of Toulouse(CRCT)ToulouseFrance UMR 152 Pharma Dev Universite de ToulouseIRDUPSToulouseFrance UMR CNRS 5089 Institut de Pharmacologie et de Biologie Structurale(IPBS)ToulouseFrance

Factors released by surrounding cells such as cancer-associated mesenchymal stromal cells(CA-MSCs)are involved in tumor progression and chemoresistance.In this study,we characterize the mechanisms by which naYve mesenchymal stromal cells(MSCs)can acquire a CA-MSCs phenotype.Ovarian tumor cells trigger the transformation of MSCs to CA-MSCs by expressing pro-tumoral genes implicated in the chemoresistance of cancer cells,resulting in the secretion of high levels of CXC chemokine receptors 1 and 2(CXCR1/2)ligands such as chemokine(C-X-C motif)ligand 1(CXCL1),CXCL2,and interleukin 8(IL-8).CXCR1/2 ligands can also inhibit the immune response against ovarian tumor cells.Indeed,through their released factors,CA-MSCs promote the differentiation of monocytes towards M2 macrophages,which favors tumor progression.When CXCR1/2 receptors are inhibited,these CA-MSC-activated macrophages lose their M2 properties and acquire an anti-tumoral phenotype.Both ex vivo and in vivo,we used a CXCR1/2 inhibitor to sensitize ovarian tumor cells to carboplatin and circumvent the pro-tumoral effects of CA-MSCs.Since high concentrations of CXCR1/2 ligands in patients*blood are associated with chemoresistance,CXCR1/2 inhibition could be a potential therapeutic strategy to revert carboplatin resistance.

关键词： chemoresistance macrophages mesenchymal stromal cells ovarian adenocarcinoma chemokines

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Mutant p53 in cancer therapy-the barrier or the path

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Journal of Molecular Cell Biology 2019年第4期11卷 293-305页

作者： Xiang Zhou Qian Hao Hua Lu Fudan University Shanghai Cancer Center and Institutes of Biomedical Sciences and Key Laboratory of Medical Epigenetics and Metabolism Fudan University Shanghai 200032 China Fudan University Shanghai Cancer Center Fudan University Shanghai 200032 China Department of Biochemistry & Molecular Biology and Tulane Cancer Center Tulane University School of Medicine New Orleans LA 70112 USA

Since wild-type p53 is central for maintaining genomic stability and preventing oncogenesis, its coding gene TP53 is highly mutated in ~50% of human cancers, and its activity is almost abrogated in the rest of cancers. Approximately 80% of p53 mutations are single point mutations with several hotspot mutations. Besides loss of function and dominant-negative effect on the wild-type p53 activity, the hotspot p53 mutants also acquire new oncogenic functions, so-called ‘gain-of-functions’(GOF). Because the GOF of mutant p53 is highly associated with late-stage malignance and drug resistance, these p53 mutants have become hot targets for developing novel cancer therapies. In this essay, we review some recent progresses in better understanding of the role of mutant p53 GOF in chemoresistance and the underlying mechanisms, and discuss the pros and cons of targeting mutant p53 for the development of anti-cancer therapies.

关键词： mutant p53 gain-of-function cancer therapy chemoresistance synthetic lethality

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Negative auto-regulators trap p53 in their web

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Journal of Molecular Cell Biology 2017年第1期9卷 62-68页

作者： Xiang Zhou Bo Cao Hua Lu Fudan University Shanghai Cancer Center and the Institutes of Biomedical Sciences Fudan University Shanghai 200032 China Department of Biochemistry & Molecular Biology and Tulane Cancer Center Tulane University School of Medicine New Orleans LA 70112 USA

transcriptional 因素 p53 激活包含一个复杂发信号网络的无数目标基因的表达式，导致各种各样的细胞的结果，并且导致瘤生长和前进的作为结果的抑制，例如生长拘捕，老朽， apoptosis，和新陈代谢的变化。因为癌症房间的生长和增长上的... 详细信息

transcriptional 因素 p53 激活包含一个复杂发信号网络的无数目标基因的表达式，导致各种各样的细胞的结果，并且导致瘤生长和前进的作为结果的抑制，例如生长拘捕，老朽， apoptosis，和新陈代谢的变化。因为癌症房间的生长和增长上的 p53 的深刻地不利的效果，几反馈机制被房间采用了抑制 p53 活动。二主要对手 MDM2 和 MDMX (长形式) 被 p53 transcriptionally 导致，但是在回来堵住 p53 活动，形成一个否定反馈电路并且显示几个癌症房间的 chemoresistance。然而，当癌症房间也采用 p53 目标基因编码在 transcriptional 禁止 p53 活动的另外的蛋白质，他们不是独自一个的，翻译，并且 posttranslational 层次。这篇散文因此被填写在理解癌症细胞怎么为他们的生长优点由这些蛋白质劫持 p53 自动调整的机制考察最近的进步并且讨论这些自动调整的环的临床的含意。

关键词： p53 MDM2 NGFR 抄写反馈循环 chemoresistance

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Glioblastoma stem cells resistant to temozolomide-induced autophagy

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Chinese Medical Journal 2009年第11期122卷 1255-1259页

作者： FU Jun LIU Zhi-gang LIU Xiao-mei CHEN Fu-rong SHI Hong-liu PANG Jesse Chung-sean NG Ho-keung CHEN Zhong-ping State Key Laboratory for Cancer Research in Southern China and Department of Neurosurgery/Neuro-oncology Cancer Center Sun Yat-sen University Guangzhon Guangdong 510060 China Department of Anatomical & Cellular Pathology Chinese University of Hong Kong Shatin N.T. Hong Kong China

Background Recent studies have demonstrated the existence of a small fraction of cells with features of primitive neural progenitor cells and tumor-initiating function in brain tumors. These cells might represent primary therapeutic target for complete eradication of the tumors. This study aimed to determine the resistant phenotype of glioblastoma stem cells （GSCs） to temozolomide （TMZ） and to explore the possible molecular mechanisms underlying TMZ resistance. Methods Freshly resected glioblastoma specimen was collected and magnetic isolation of GSCs was carried out using the Miltenyi Biotec CD133 Cell Isolation kit. The cytotoxic effect of TMZ on CD133^＋ and CD133^- glioblastoma cells was determined by using the 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyltetrazolium bromide （MTT） assay. Autophagy-related proteins （Beclin-1, LC3 and Atg5） and cleaved caspase-3 （p17） were analyzed by Western blotting. Immunofluorescent staining was used to detect Atg5, glial fibrillary acidic protein （GFAP） and CD133 expression in glioblastoma cells. Statistical analysis was carried out using SPSS 10.0 software. For all tests, the level of statistical significance was set at P 〈0.05. Results CD133^＋ glioblastoma ceils exhibited neurosphere-like growth in vitro and high expression of CD133 stem cell marker. The growth-inhibiting rate in CD133- glioblastoma cells treated with 5 or 50 pmol/L TMZ was significantly higher than that in CD133^＋ glioblastoma cells （（14.36±3.75）% vs （2.54±1.36）% or （25.95±5.25）% vs （2.72±1.84）%, respectively, P 〈0.05）. Atg5, LC3-11 and Beclin-1 levels were significantly lower in CD133^＋ glioblastoma cells than those in autologous CD133^- cells after TMZ treatment （P 〈0.05）. Caspase-3 was mildly activated only in CD133^- glioblastoma cells after exposure to TMZ （P 〈0.05）. Immunofluorescent staining revealed elevated expression of Atg5 in GFAP^＋ cells following TMZ treatment. Conclusions The GSCs display strong capability of tumor＇s resistance to TMZ. This resistance is probably contributed by the CD133^＋ cel

关键词： glioblastoma neoplastic stem cells chemoresistance temozolomide

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Adenovirus Mediated BIMS Transfer Induces Growth Supression and Apoptosis in Raji Lymphoma Cells

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Biomedical and Environmental Sciences 2014年第9期27卷 655-664页

作者： ZHAO Ya Ning LI Qiang Department of Pediatric Hematology and Immunology West China Second University HospitalSichuan University. Key Laboratory of Birth Defects and Related Diseases of Women and Children (Sichuan University)Ministry of Education Department of Phymatology Baoji Municipal Central Hospital

Objective To transfer pro-apoptotic BIM directly into tumor cells bypass the complicated biologica processes of BIM activation so as to reverse the chemoresistance of cancer cells. Methods BIMS was specifically amplified from HL-60 cells by RT-PCR, confirmed to be correct by sequencing and cloned into shuttle vector pAdTrack-CMV carrying a green fluorescence protein gene to generate a recombinant plasmid pAdTrack-CMV-BIMS. This plasmid and adenovirus backbone plasmid pAdEasy-1 were linearized and electroporated into E.coli BJ5183 host bacteria to mediate homologous recombination. The positive clone was identified by restrict endonuclease digestion. The recombinant pAdEasy-CMV-BIMS was transferred into HEK293 cells for packaging and amplification. The successful construction of recombinant human BIMS adenovirus （Ad-BIMS） was demonstrated by Western blot. To test whether Ad-BIMS has the capability of inducing apoptosis of tumor cells, Ad-BIMS was used to infect GC resistant Burkitt lymphoma Raji cells. Results After infected for 2-5 days, BIMS expression in Raji cells was detected by RT-PCR and Western blot. The significant growth retardation and apoptosis of Raji cells were also observed by MTI- and flow cytometry. Conclusion These results indicated that BIMS might be a potential candidate of gene therapy for chemoresistant tumor cells.

关键词： BIMS chemoresistance Gene therapy Recombinant adenovirus Transfection Lymphoma Apoptosis Tumor

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chemoresistance is associated with overexpression of HAX-1,inhibition of which resensitizes drug-resistant breast cancer cells to chemotherapy

Chemoresistance is associated with overexpression of HAX-1,i...

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2019年浙江省医学会中毒学学术大会

作者：杨霁

Acquired resistance to standard chemotherapy is the common and critical limitation for cancer therapy.Hematopoietic cell-specific protein 1-associated protein X-1(HAX-1) has been reported to be upregulated in numerous cancers.However,the role of HAX-1 in oncotherapy remains unclear.In this study,we established MDAMB-231 cell lines which were resistant to cisplatin(MDA-MB-231/CR) or doxorubicin(MDA-MB-231/DR) to study the chemoresistance in breast cancer.As a result,the HAX-1 which was used as an apoptosis-associated protein was observed to be overexpressed in both MDA-MB-231/CR and MDA-MB-231/DR compared with the routine MDAMB-231 cells.Moreover,knockdown of HAX-1 via RNA interference decreased IC50 level of cisplatin by 70.91%in MDA-MB-231/CR cells,and the IC50 level of doxorubicin was decreased by 76.46% in MDA-MB-231/DR cells when the HAX-1 was downregulated.Additionally,we found that the knockdown of HAX-1 induced the release of cytochrome C from mitochondria,resulting in the activation of caspases.Taken together,our study indicates that the overexpression of HAX-1 is essential in the development of chemoresi stance in breast cancer.Furthermore,we identify that HAX-1 may become a target for cancer therapy.

关键词： HAX-1 chemoresistance chemotherapeutics apoptosis breast cancer

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Tim-3 promotes cell aggressiveness and paclitaxel resistance through NF-κB/STAT3 signalling pathway in breast cancer cells

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Chinese Journal of Cancer Research 2020年第5期32卷 564-579页

作者： Yizi Cong Yuxin Cui Shiguang Zhu Jianqiao Cao Haidong Zou Tracey AMartin Guangdong Qiao Wenguo Jiang Zhigang Yu Department of Breast Surgery The Second HospitalCheeloo College of MedicineShandong UniversityJinan 250033China Department of Breast Surgery The Affiliated Yantai Yuhuangding Hospital of Qingdao UniversityYantai 264001China Cardiff China Medical Research Collaborative School of MedicineCardiff UniversityCardiffCF144XNUK

Objective:Although T-cell immunoglobulin and mucin-domain containing molecule-3(Tim-3)has been recognized as a promising target for cancer immunotherapy,its exact role in breast cancer has not been fully elucidated.Methods:Tim-3 gene expression in breast cancer and its prognostic significance were analyzed.Associated mechanisms were then explored in vitro by establishing Tim-3-overexpressing breast cancer cells.Results:In a pooled analysis of The Cancer Genome Atlas(TCGA)database,Tim-3 gene expression levels were significantly higher(P<0.001)in breast cancer tissue,compared with normal tissues.Tim-3 was a prognosis indicator in breast cancer patients[relapse-free survival(RFS),P=0.004;overall survival(OS),P=0.099].Tim-3 overexpression in Tim-3 low breast cancer cells promoted aggressiveness of breast cancer cells,as evidenced by enhanced proliferation,migration,invasion,tight junction deterioration and tumor-associated tubal formation.Tim-3 also enhanced cellular resistance to paclitaxel.Furthermore,Tim-3 exerted its function by activating the NF-κB/STAT3 signalling pathway and by regulating gene expression[cyclin D1(CCND1),C-Myc,matrix metalloproteinase-1(MMP1),TWIST,vascular endothelial growth factor(VEGF)upregulation,concomitant with Ecadherin downregulation).Lastly,Tim-3 downregulated tight junction-associated molecules zona occludens(ZO)-2,ZO-1 and occludin,which may further facilitate tumor progression.Conclusions:Tim-3 plays an oncogenic role in breast cancer and may represent a potential target for antitumor therapy.

关键词： Breast neoplasm hepatitis A virus cellular receptor 2 tight junction aggression chemoresistance

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