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The transcription factor ZEB1 promotes chemoresistance in prostate cancer cell lines

Asian Journal of Andrology 2019年第5期21卷 460-467页

作者： Octavio Orellana-Serradell Daniela Herrera Enrique A Castellon Hector R Contreras Department of Basic and Clinical Oncology Faculty of MedicineUniversity of ChileIndependenciaSantiago 8380453Chile

One of the factors promoting tumoral progress is the abnormal activation of the epithelial-mesenchymal transition(EMT)program which has been associated with chemoresistance in tumoral cells.The transcription factor zinc finger E-box-binding homeobox 1(ZEB1),a key EMT activator,has recently been related to docetaxel resistance,the main chemotherapeutic used in advanced prostate cancer treatment.The mechanisms involved in this protective effect are still unclear.In a previous work,we demonstrated that ZEB1 expression induced an EMT-like phenotype in prostate cancer cell lines.In this work,we used prostate cancer cell lines 22Rvl and DU145 to study the effect of ZEB1 modulation on docetaxel resistance and its possible mechanisms.The results showed that ZEB1 overexpression conferred to 22Rvl cell resistance to docetaxel while its silencing made DU145 cells more sensitive to it.Analysis of resistance markers showed no presenee of ATP-binding cassette subfamily B member 1(MDR1)and no changes in breast cancer resistance protein(BCRP)or ATP-binding cassette subfamily C member 10(MRP7).However,a correlation between ZEB1,multidrug resistance-associated protein 1(MRP1),and ATP-binding cassette subfamily C member 4(MRP4)expression was observed.MRP4 inhibition,using MK571,resensitized cells with ZEB1 overexpression to docetaxel treatment.In addition,modulation of ZEB1 and subsequent change in MRP4 expression correlated with a lower apoptotic response to docetaxel,characterized by lower B-cell lymphoma 2(Bcl2),high BCL2-associated X protein(Bax),and high active caspase 3 expression.The response to docetaxel in our model seems to be mediated mainly by activation of the apoptotic death program.Our results showed that modulation of MRP4 could be a mediator of ZEBl-related resistance to docetaxel in prostate cancer,making it a possible marker for chemotherapy response in patients who do not express MDR1.

关键词： chemoresistance prostate cancer ZEB1

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Down.regulation of E.cadherin enhances prostate cancer chemoresistance via Notch signaling

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Chinese Journal of Cancer 2017年第3期36卷 150-162页

作者： Wenchu Wang Lihui Wang Atsushi Mizokami Junlin Shi Chunlin Zou Jinlu Dai Evan T. Keller Yi Lu Jian Zhang Center for Translational Medicine Guangxi Medical University 12th FloorMedical Science Research Building No. 22 Shuangyong Road NanningGuangxi 530021 P. R. China Key Laboratory of Longevity and Ageingrelated Diseases Ministry of Education Nanning Guangxi 530021 P. R. China Department of Urology and Pathology School of Medicine University of Michigan Ann Arbor MI 48109 USA Department of Urology Graduate School of Medical Sciences Kanazawa University Kanazawa 920.1192 Japan Department of Biology and School of Medicine Southern University of Science and Technology Shenzhen Guangdong 518055 P. R. China Department of Urology University of Pittsburgh School of Medicine Pittsburgh PA 15232 USA

Background:The chemoresistance of prostate cancer(PCa)is invariably associated with the aggressiveness and metastasis of this disease.New emerging evidence indicates that the epithelial-to-mesenchymal transition(EMT)may play pivotal roles in the development of chemoresistance and metastasis.As a hallmark of EMT,E-cadherin is suggested to be a key marker in the development of chemoresistance.However,the molecular mechanisms underlying PCa chemoresistance remain unclear.The current study aimed to explore the association between EMT and chemoresistance in PCa as well as whether changing the expression of E-cadherin would affect PCa chemoresistance.Methods:Parental PC3 and DU145 cells and their chemoresistant PC3-Tx R and DU145-Tx R cells were analyzed.PC3-Tx R and DU145-Tx R cells were transfected with E-cadherin-expressing lentivirus to overexpress E-cadherin;PC3 and DU145 cells were transfected with small interfering RNA to silence E-cadherin.Changes of EMT phenotype-related markers and signaling pathways were assessed by Western blotting and quantitative real-time polymerase chain reaction.Tumor cell migration,invasion,and colony formation were then evaluated by wound healing,transwell,and colony formation assays,respectively.The drug sensitivity was evaluated using MTS assay.Results:Chemoresistant PC3-Tx R and DU145-Tx R cells exhibited an invasive and metastatic phenotype that associated with EMT,including the down-regulation of E-cadherin and up-regulation of Vimentin,Snail,and N-cadherin,comparing with that of parental PC3 and DU145 cells.When E-cadherin was overexpressed in PC3-Tx R and DU145-Tx R cells,the expression of Vimentin and Claudin-1 was down-regulated,and tumor cell migration and invasion were inhibited.In particular,the sensitivity to paclitaxel was reactivated in E-cadherin-overexpressing PC3-Tx R and DU145-Tx R cells.When E-cadherin expression was silenced in parental PC3 and DU145 cells,the expression of Vimentin and Snail was up-regulated,and,particularly,the sensitivity to paclitaxel was dec

关键词： Epithelial-to-mesenchymal transition E-cadherin chemoresistance Notch signaling Prostate cancer

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p53 deficiency-induced Smad1 upregulation suppresses tumorigenesis and causes chemoresistance in colorectal cancers

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分子细胞生物学报:英文版 2015年第2期7卷 105-118页

作者： Xinsen Ruan Qiao Zuo Hao Jia Jenny Chau Jinlin Lin Junping Ao Xuechun Xia Huijuan Liu Samy LHabib Chuangang Fu Baojie Li Bio-X Institutes Key Laboratory for the Genetics of Developmental and Neuropsychiatric DisordersMinistry of EducationShanghai Jiao Tong UniversityShanghai 200240China Department of Colorectal Surgery Changhai HospitalSecond Military Medical UniversityShanghai 200433China Institute of Molecular and Cell Biology Proteos61 Biopolis DriveSingapore 138673Singapore State Key Laboratory of Oncogenes and Related Genes Shanghai Cancer InstituteRenji HospitalShanghai Jiao Tong UniversitySchool of MedicineShanghai 200032China Department of Cellular and Structural Biology University of Texas Health Science Center at San AntonioSan AntonioTX 78229USA

The DNA damage response helps to maintain genome integrity,suppress tumorigenesis,and mediate the effects of radiotherapy and chemotherapy.Our previous studies have shown that Smad1 is upregulated and activated by Atm in DNA damage response,which can further bind to p53 and promote p53 stabilization.Herewe report another aspect of the interplay between p53 and Smad1.Comparison of rectal tumor against paired paraneoplastic specimens and analysis of>500 colorectal tumors revealed that Smad1 was upregulated in tumor samples,which was attributable to p53 defects.Using MEFs as a model,we found that knockdown of the elevated Smad1 in p532/2 MEFs promoted cell proliferation,E1A/Ras-induced cell transformation,and tumorigenesis.Mechanistic studies suggest that elevated Smad1 and momentary activation inhibit cell proliferation by upregulating p57Kip2 and enhancing Atm–Chk2 activation.Surprisingly,elevated Smad1 appears to have a negative effect on chemotherapy,as colorectal tumors,primary cancer cells,and cell lines with Smad1 knockdown all showed an increase in chemosensitivity,which could be attributable to elevated p57Kip2.These findings underscore the significance of Smad1–p53 interaction in tumor suppression and reveal an unexpected role for Smad1 in chemoresistance of colorectal cancers.

关键词： Smad1 p53 p57Kip2 chemoresistance colorectal cancer

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Upregulation of Neural Precursor Cell Expressed Developmentally Downregulated 4-1 is Associated with Poor Prognosis and chemoresistance in Lung Adenocarcinoma

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Chinese Medical Journal 2018年第1期131卷 16-24页

作者： Ying-Hua Song Cai-Qing Zhang Fang-Fang Chen Xiao-Yan Lin Department of Respiratory Medicine Shandong Qianfoshan Hospital Shandong University Jinan Shandong 250014 China Department of Pathology Shandong Provincial Hospital Affiliated to Shandong University Jinan Shandong 250021 China

Background： The E3 ubiquitin ligasc neural precursor cell expressed developmentally downregulated 4-1（N EDD4-1） negatively regulates phosphatase and tensin homolog deleted on chromosome 10 （PTEN） protein levels through polyubiquitination and proteolysis, but its significance in lung cancer is still unclear. This study investigated the expression and the role of NEDD4-1 in tumor developnaent and chemosensitivity of lung adenocarcinoma （ADC）. Methods： We retrospectively investigated the expression and significance ofNEDD4-1, PTEN, and p-Akt proteins in 135 paired A DC and adjacent noncancerous tissue specimens using immunohistochemistry. Furthemaore, we evaluated the relationship between NEDD4-1 expression and clinicopathologic characteristics and prognosis. The effects of small interfering RNA against NEDD4-1 on proliferation and chemosensitivity were examined in A549 cells in vitro using 3- （4,5-dimethylthiazol-2-yl） -5-（3-carboxymethoxyphenyl） -2-（4-sulfophenyl）- 2H-tetrazoliunl method. The ability of migration and invasion ofA549 cells was tested by transwell assay. Moreover, reverse-transcription quantitative polymerase chain reaction and Western blotting analyses were used to determine the expression of NEDD4-1, PTEN, phosphoinositide 3-kinase （PI3K）/Akt activity, and its downstream target proteins. Results： NEDD4-1 protein was significantly upregulated in lung ADC tissues, whereas it was weak or negative in normal lung epithelial cells. The expression ofNEDD4-1 in ADC （78.5%, 106/135） was significantly much higher than that in adjacent normal lung tissue （ 13.3%, 29/135, P 〈 0.01）, and it was associated with lymph node metastasis, tumor-node-metastasis （TNM） stage, and chemotherapy resistance. PTEN expression was downregulated in lung ADC （60.7% vs. 100.0% in noncancerous specimens, P - 0.007）, and was negatively correlated with lymph node metastasis, histological variants, clinical stage, chemoresistance. In addition, expression of p-Akt in ADC tissues （71.1% 96/135） was much higher than that in adjacent lu

关键词： chemoresistance Lung Adenocarcinoma： NEDD4-1： PTEN 10 Prognosis

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Hepatitis B core antigen modulates exosomal miR-135a to target vesicle-associated membrane protein 2 promoting chemoresistance in hepatocellular carcinoma

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World Journal of Gastroenterology 2021年第48期27卷 8302-8322页

作者： Xiao-Cui Wei Ya-Ru Xia Ping Zhou Xing Xue Shuang Ding Li-Juan Liu Fan Zhu State Key Laboratory of Virology Hubei Province Key Laboratory of Allergy and ImmunologyDepartment of Medical MicrobiologySchool of MedicineWuhan UniversityWuhan 430071Hubei ProvinceChina

BACKGROUND Hepatocellular carcinoma(HCC)is one of the most common malignant tumors.The association of hepatitis B virus(HBV)infection with HCC is hitherto documented.Exosomal miRNAs contribute to cancer progression and chemoresistance.HBV X protein has been known to modulate miRNAs that facilitate cell proliferation and the process of hepatocarcinogenesis.However,there has been no report on hepatitis B core antigen(HBc)regulating exosomal miRNAs to induce drug resistance of HCC cells.AIM To elucidate the mechanism by which HBc promotes Doxorubicin hydrochloride(Dox)resistance in HCC.METHODS Exosomes were isolated by ultracentrifugation.The morphology and size of exosomes were evaluated by Dynamic Light Scattering(DLS)and transmission electron microscopy(TEM).The miRNAs differentially expressed in HCC were identified using The Cancer Genome Atlas(TCGA)database.The level of miR-135a-5p in patient tissue samples was detected by quantitative polymerase chain reaction.TargetScan and luciferase assay were used to predict and prove the target gene of miR-135a-5p.Finally,we identified the effects of miR-135a-5p on anti-apoptosis and the proliferation of HCC in the presence or absence of Dox using flow cytometry,Cell counting kit 8(CCK-8)assay and western blot.RESULTS We found that HBc increased the expression of exosomal miR-135a-5p.Integrated analysis of bioinformatics and patient samples found that miR-135a-5p was increased in HCC tissues in comparison with paracancerous tissues.Bioinformatic analysis and in vitro validation identified vesicle-associated membrane protein 2(VAMP2)as a novel target gene of miR-135a-5p.Functional assays showed that exosomal miR-135a-5p induced apoptosis protection,cell proliferation,and chemotherapy resistance in HCC.In addition,the rescue experiment demonstrated that VAMP2 reversed apoptosis protection,cell growth,and drug resistance by miR-135a-5p.Finally,HBc promoted HCC anti-apoptosis,proliferation,and drug resistance and prevented Dox-induced apoptosis via the miR-135a-5p/VAMP2 axis.

关键词： Hepatocellular carcinoma Exosomes miR-135a-5p Anti-apoptosis Proliferation chemoresistance

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Zinc oxide nanoparticles reduce the chemoresistance of gastric cancer by inhibiting autophagy

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World Journal of Gastroenterology 2021年第25期27卷 3851-3862页

作者： You-Han Miao Li-Ping Mao Xiao-Juan Cai Xiao-Ying Mo Qi-Qi Zhu Fei-Tong Yang Mei-Hua Wang Department of Infectious Disease Nantong Third People’s HospitalNantong 226006Jiangsu ProvinceChina

BACKGROUND Gastric cancer(GC)is a common malignancy that results in a high rate of cancerrelated mortality.Cisplatin(DDP)-based chemotherapy is the first-line clinical treatment for GC therapy,but chemotherapy resistance remains a severe clinical challenge.Zinc oxide nanoparticle(ZnO-NP)has been identified as a promising anti-cancer agent,but the function of ZnO-NP in GC development is still unclear.AIM To explore the effect of ZnO-NP on chemotherapy resistance during GC progression.METHODS ZnO-NP was synthesized,and the effect and underlying mechanisms of ZnO-NP on the malignant progression and chemotherapy resistance of GC cells were analyzed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT)assays,colony formation assays,transwell assays,wound healing assays,flow cytometry,and Western blot analysis in GC cells and DDP-resistant GC cells,and by tumorigenicity analyses in nude mice.RESULTS Our data revealed that ZnO-NP was able to inhibit proliferation,migration,and invasion and induce apoptosis of GC cells.Meanwhile,ZnO-NP significantly reduced the half maximal inhibitory concentration(IC50)of DDP for the inhibition of cell proliferation of DDP-resistant SGC7901/DDP cell lines.Autophagy was increased in DDP-resistant GC cells,as demonstrated by elevated light chain 3-like protein 2(LC3II)/LC3I and Beclin-1 expression and repressed p62 expression in SGC7901/DDP cells compared to SGC7901 cells.Mechanically,ZnO-NP inhibited autophagy in GC cells and treatment with DDP induced autophagy,which was reversed by ZnO-NP.Functionally,ZnO-NP attenuated the tumor growth of DDP-resistant GC cells in vivo.CONCLUSION We conclude that ZnO-NP alleviates the chemoresistance of GC cells by inhibiting autophagy.Our findings present novel insights into the mechanism by which ZnO-NP regulates the chemotherapy resistance of GC.ZnO-NP may serve as a potential therapeutic candidate for GC treatment.The potential role of ZnO-NP in the clinical treatment of GC needs clarification in future investigations.

关键词： Gastric cancer Progression chemoresistance Zinc oxide nanoparticle Autophagy MTT assays

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Glutathione metabolism is essential for self-renewal and chemoresistance of pancreatic cancer stem cells

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World Journal of Stem Cells 2020年第11期12卷 1410-1428页

作者： Petra Jagust Sonia Alcala Bruno Sainz Jr Christopher Heeschen Patricia Sancho Molecular Pathology Programme Spanish National Cancer Research Centre(CNIO)Madrid 28029Spain Department of Biochemistry Autónoma University of MadridInstituto de Investigaciones Biomédicas"Alberto Sols"CSIC-UAMMadrid 28029Spain Center for Single-Cell Omics&Key Laboratory of Oncogenes and Related Genes Shanghai Cancer InstituteShanghai Jiao Tong University School of MedicineShanghai 200025China Hospital Universitario Miguel Servet IIS AragonZaragoza 50009Spain

BACKGROUND Cellular metabolism regulates stemness in health and disease.A reduced redox state is essential for self-renewal of normal and cancer stem cells(CSCs).However,while stem cells rely on glycolysis,different CSCs,including pancreatic CSCs,favor mitochondrial metabolism as their dominant energy-producing pathway.This suggests that powerful antioxidant networks must be in place to detoxify mitochondrial reactive oxygen species(ROS)and maintain stemness in oxidative CSCs.Since glutathione metabolism is critical for normal stem cell function and CSCs from breast,liver and gastric cancer show increased glutathione content,we hypothesized that pancreatic CSCs also rely on this pathway for ROS detoxification.AIM To investigate the role of glutathione metabolism in pancreatic CSCs.METHODS Primary pancreatic cancer cells of patient-derived xenografts(PDXs)were cultured in adherent or CSC-enriching sphere conditions to determine the role of glutathione metabolism in stemness.Real-time polymerase chain reaction(PCR)was used to validate RNAseq results involving glutathione metabolism genes in adherent vs spheres,as well as the expression of pluripotency-related genes following treatment.Public TCGA and GTEx RNAseq data from pancreatic cancer vs normal tissue samples were analyzed using the webserver GEPIA2.The glutathione-sensitive fluorescent probe monochlorobimane was used to determine glutathione content by fluorimetry or flow cytometry.Pharmacological inhibitors of glutathione synthesis and recycling[buthionine-sulfoximine(BSO)and 6-Aminonicotinamide(6-AN),respectively]were used to investigate the impact of glutathione depletion on CSC-enriched cultures.Staining with propidium iodide(cell cycle),Annexin-V(apoptosis)and CD133(CSC content)were determined by flow cytometry.Self-renewal was assessed by sphere formation assay and response to gemcitabine treatment was used as a readout for chemoresistance.RESULTS Analysis of our previously published RNAseq dataset E-MTAB-3808 revealed upregulation of genes involved in

关键词： Pancreatic cancer Cancer stem cells Glutathione Self-renewal chemoresistance Redox

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Lipid droplets as metabolic determinants for stemness and chemoresistance in cancer

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World Journal of Stem Cells 2021年第9期13卷 1307-1317页

作者： Alba Royo-Garcia Sarah Courtois Beatriz Parejo-Alonso Pilar Espiau-Romera Patricia Sancho Hospital Universitario Miguel Servet IIS AragónZaragoza 50009Spain

Previously regarded as simple fat storage particles,new evidence suggests thatlipid droplets(LDs)are dynamic and functional organelles involved in keycellular processes such as membrane biosynthesis,lipid metabolism,cellsignalling and inflammation.Indeed,an increased LD content is one of the mostapparent features resulting from lipid metabolism reprogramming necessary tosupport the basic functions of cancer cells.LDs have been associated to differentcellular processes involved in cancer progression and aggressiveness,such astumorigenicity,invasion and metastasis,as well as chemoresistance.Interestingly,all of these processes are controlled by a subpopulation of highly aggressivetumoral cells named cancer stem cells(CSCs),suggesting that LDs may befundamental elements for stemness in cancer.Considering the key role of CSCs onchemoresistance and disease relapse,main factors of therapy failure,the design ofnovel therapeutic approaches targeting these cells may be the only chance forlong-term survival in cancer patients.In this sense,their biology and functionalproperties render LDs excellent candidates for target discovery and design ofcombined therapeutic strategies.In this review,we summarise the currentknowledge identifying LDs and CSCs as main contributors to cancer aggressiveness,metastasis and chemoresistance.

关键词： Lipids Lipid droplets Lipid metabolism Stemness Cancer stem cells chemoresistance

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VPS33B suppresses lung adenocarcinoma metastasis and chemoresistance to cisplatin

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Genes & Diseases 2021年第3期8卷 307-319页

作者： Zhen Liu Jiahao Liu Yang Li Hao Wang Zixi Liang Xiaojie Deng Qiaofen Fu Weiyi Fang Ping Xu Affiliated Cancer Hospital&Institute of Guangzhou Medical University Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and DegradationState Key Laboratory of Respiratory DiseaseSchool of Basic Medical SciencesGuangzhou Medical UniversityGuangzhouGuangdong Province510095PR China Cancer Center Integrated Hospital of Traditional Chinese MedicineSouthern Medical UniversityGuangzhouGuangdong Province510310PR China Cancer Institute School of Basic Medical SciencesSouthern Medical UniversityGuangzhouGuangdong Province510515PR China Respiratory Department Peking University Shenzhen HospitalShenzhenGuangdong Province518034PR China

The presence of VPS33B in tumors has rarely been reported.Downregulated VPS33B protein expression is an unfavorable factor that promotes the pathogenesis of lung adenocar-cinoma(LUAD).Overexpressed VPS33B was shown to reduce the migration,invasion,metas-tasis,and chemoresistance of LUAD cells to cisplatin(DDP)in vivo and in vitro.Mechanistic analyses have indicated that VPS33B first suppresses epidermal growth factor receptor(EGFR)Ras/ERK signaling,which further reduces the expression of the oncogenic factor C-Myc.Down-regulated c-Myc expression reduces the rate at which it binds the p53 promoter and weakens its transcription inhibition;therefore,decreased C-Myc stimulates p53 expression,leading to decreased epithelial-to-mesenchymal transition(EMT)signal.NESG1 has been shown to be an unfavorable indicator of non-small-cell lung cancer(NSCLC).Here,NESG1 Was identified as an interactive protein of VPS33B.In addition,NESG1 was found to exhibit mutual stimulation with VPS33B via reduced RAS/ERK/c-Jun-mediated transcription repression.Knockdown of NESG1 activated EGFR/Ras/ERK/c-Myc signaling and further downregulated p53 expression,which thus activated EMT signaling and promoted LUAD migration and invasion.Finally,we observed that nicotine suppressed VPS33B expression by inducing PI3K/AKT/c-Jun-mediated transcription suppression.Our study demonstrates that VPS33B as a tumor suppressor is signif-icantly involved in the pathogenesis of LUAD.

关键词： chemoresistance Lung adenocarcinoma Metastasis Nicotine VPS33B

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Attempts to remodel the pathways of gemcitabine metabolism: Recent approaches to overcoming tumours with acquired chemoresistance

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Cancer Drug Resistance 2020年第4期3卷 819-831页

作者： Yuriko Saiki Shuto Hirota Akira Horii Department of Molecular Pathology Tohoku University School of MedicineSendaiMiyagi 980-8575Japan Office of Medical Education Tohoku University School of MedicineSendaiMiyagi 980-8575Japan Saka General Hospital ShiogamaMiyagi 985-0024Japan

Gemcitabine is a cytidine analogue frequently used in the treatment of various cancers.However,the development of chemoresistance limits its effectiveness.Gemcitabine resistance is regulated by various factors,including aberrant genetic and epigenetic controls,metabolism of gemcitabine,the microenvironment,epithelial-to-mesenchymal transition,and acquisition of cancer stem cell properties.In many situations,results using cell lines offer valuable lessons leading to the first steps of important findings.In this review,we mainly discuss the factors involved in gemcitabine metabolism in association with chemoresistance,including nucleoside transporters,deoxycytidine kinase,cytidine deaminase,and ATP-binding cassette transporters,and outline new perspectives for enhancing the efficacy of gemcitabine to overcome acquired chemoresistance.

关键词： Gemcitabine chemoresistance deoxycytidine kinase human equilibrative nucleoside transporter 1 cytidine deaminase ATP-binding cassette transporters metabolism

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