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Akt isoforms differentially provide for Chemoresistance in prostate cancer

Cancer Biology & Medicine 2022年第5期19卷 635-650页

作者： Bo Ma Hanshuang Shao Xia Jiang Zhou Wang Chuanyue(Cary)Wu Diana Whaley Alan Wells Jiangsu Center for the Collaboration and Innovation of Cancer Biotherapy Cancer InstituteXuzhou Medical UniversityXuzhou 221002China Department of Pathology University of PittsburghPittsburghPA 15261USA Pittsburgh VA Healthcare System PittsburghPA 15213USA Department of Biomedical Informatics University of PittsburghPittsburghPA 15261USA Department of Urology University of PittsburghPittsburghPA 15261USA Department of Pharmacology and Chemical Biology University of PittsburghPittsburghPA 15261USA UPMC Hillman Cancer Center PittsburghPA 15232USA

Objective:Early prostate cancer micrometastatic foci undergo a mesenchymal to epithelial reverting transition,not only aiding seeding and colonization,but also rendering the tumor cells generally chemoresistant.We previously found that upregulated E-cadherin in the epithelial micrometastases activated canonical survival pathways,including PI3K-Akt,that protected the tumor cells from death;however,the extent of protection from blocking the pathway in its entirety was modest,because different isoforms may have alternately affected cell functioning.Here,we characterized Akt isoform expressions in primary and metastatic prostate cancers,as well as their individual contributions to Chemoresistance.Methods:Akt isoforms and E-cadherin were manipulated with drugs,knocked down,and over expressed.Tumor cell killing was determined in vitro and in vivo.Overall survival was calculated from patient records and specimens.Results:Pan-Akt inhibition sensitized tumor cells to chemotherapy,and specific blockade of Akt1 or/and Akt2 caused cells to be more chemoresponsive.Overexpression of Akt3 induced apoptosis.A low dose of Akt1 or Akt2 inhibitor enabled standard chemotherapies to significantly eradicate metastatic prostate tumors in a mouse model,acting as chemosensitizers.In human specimens,we found Akt1 and Akt2 positively correlated,whereas Akt3 inversely correlated,with the overall survival of prostate cancer patients.Akt1high/Akt2high/Akt3low tumors had the worst outcomes.Conclusions:E-cadherin-induced activation of Akt1/2 isoforms was the essential mechanism of Chemoresistance,whereas Akt3 made cells more fragile.These findings emphasized the need to target Akt1/2,rather than pan-Akt,as a rational therapeutic approach.

关键词： Chemoresistance adjuvant therapy metastasis dormancy Akt isoforms

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N^(6)-methyladenosine modification of CENPK mRNA by ZC3H13 promotes cervical cancer stemness and Chemoresistance

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Military Medical Research 2022年第5期9卷 576-591页

作者： Xian Lin Feng Wang Jian Chen Jing Liu Yi-Bin Lin Li Li Chuan-Ben Chen Qin Xu Departments of Gynecology Fujian Cancer Hospital and Fujian Medical University Cancer HospitalFujian Medical UniversityFuzhou 350014China Department of Radiation Oncology Fujian Cancer Hospital and Fujian Medical University Cancer HospitalFujian Medical UniversityFuzhou 350014China Shenzhen Key Laboratory of Immunity and Inflammatory Diseases Peking University Shenzhen HospitalShenzhen Peking University?the Hong Kong University of Science and Technology Medical CenterShenzhen 518036GuangdongChina Outpatient Department Fujian Hospital of People's Armed PoliceFujian Medical UniversityFuzhou 350014China

Background:Stemness and Chemoresistance contribute to cervical cancer recurrence and metastasis.In the current study,we determined the relevant players and role of N^(6)-methyladenine(m^(6)A)RNA methylation in cervical cancer progression.Methods:The roles of m^(6)A RNA methylation and centromere protein K(CENPK)in cervical cancer were analyzed using bioinformatics analysis.Methylated RNA immunoprecipitation was adopted to detect m^(6)A modification of CENPK mRNA.Human cervical cancer clinical samples,cell lines,and xenografts were used for analyzing gene expression and function.Immunofluorescence staining and the tumorsphere formation,clonogenic,MTT,and EdU assays were performed to determine cell stemness,Chemoresistance,migration,invasion,and proliferation in HeLa and SiHa cells,respectively.Western blot analysis,co-immunoprecipitation,chromatin immunoprecipitation,and luciferase reporter,cycloheximide chase,and cell fractionation assays were performed to elucidate the underlying mechanism.Results:Bioinformatics analysis of public cancer datasets revealed firm links between m^(6)A modification patterns and cervical cancer prognosis,especially through ZC3H13-mediated m^(6)A modification of CENPK mRNA.CENPK expression was elevated in cervical cancer,associated with cancer recurrence,and independently predicts poor patient prognosis[hazard ratio=1.413,95%confidence interval=1.078−1.853,P=0.012].Silencing of CENPK prolonged the overall survival time of cervical cancer-bearing mice and improved the response of cervical cancer tumors to chemotherapy in vivo(P<0.001).We also showed that CENPK was directly bound to SOX6 and disrupted the interactions of CENPK withβ-catenin,which promotedβ-catenin expression and nuclear translocation,facilitated p53 ubiquitination,and led to activation of Wnt/β-catenin signaling,but suppression of the p53 pathway.This dysregulation ultimately enhanced the tumorigenic pathways required for cell stemness,DNA damage repair pathways necessary for cisplatin/carboplatin resistance,epithelial-m

关键词： N^(6)-methyladenosine Centromere protein K Cervical cancer Stemness Chemoresistance

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An active RUNX1-ID1/ID3 axis governs differentiation and Chemoresistance of cancer stem cell population in epithelial ovarian cancer cells

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BIOCELL 2022年第1期46卷 75-86页

作者： AJIT CDHADVE PRITHA RAY Imaging Cell Signaling&Therapeutics Laboratory Advanced Centre for TreatmentResearch and Education in CancerTata Memorial CentreNavi Mumbai410210India Homi Bhabha National Institute Mumbai400094India

Progression,relapse,and therapy resistance are the most challenging features of cancer therapy that have been postulated to be driven by Cancer Stem Cell(CSC)population.This enigmatic subpopulation of cancer cells has therefore emerged as promising therapeutic candidate.We earlier reported enrichment of CSC-like side population(SP)with increasing resistance towards Cisplatin and Paclitaxel either alone or in combination in epithelial ovarian cancer(EOC)cells.This SP population is a small proportion of the total population of cancer cells characterised with high expression of drug transporters,a unique feature of stem cells and thereby can be isolated through their efflux properties of DNA binding dyes.While the bulk non-SP(NSP)population of the cancer cells lack overexpression of the drug transporters and thus can be identified as the dye containing population.In this study,we show that increased expression of Runt related transcription factor 1(RUNX1)maintains undifferentiated state of CSC-like SP cells through upregulation of inhibitors of DNA binding/differentiation genes(ID1 and ID3)in late cisplatinpaclitaxel resistant cells.Higher RUNX1 expression was found to correlate with decreased median overall survival and disease-free survival in The Cancer Genome Atlas(TCGA)data set of high grade serous ovarian cancer(HGSOC)patients.The protein-protein interaction network analysis of 397 upregulated genes in RUNX1-high samples of TCGA data show significant enrichment of pathways known to negatively regulate CSC differentiation.Intriguingly RUNX1 inhibition not only induces CSC differentiation but also downregulates anti-apoptotic protein BCL2 in both SP and NSP cells and potentiates cytotoxic effects of Cisplatin-Paclitaxel in chemoresistant EOC cells.Inhibition of BCL2 through Venetoclax treatment,a small molecule BH3 mimic,sensitized these cells to platinum taxol treatment.Altogether,our data reveal new regulatory roles by RUNX1 to modulate CSC differentiation via ID1 and ID3 and to promote Chemoresistance through

关键词： Cancer stem cells Differentiation RUNX1 ID1 ID2 BCL2 Chemoresistance Ovarian cancer

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Circular RNAs:new biomarkers of Chemoresistance in cancer

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Cancer Biology & Medicine 2021年第2期18卷 421-436页

作者： Jiaqi Wang Yi Zhang Lianyu Liu Ting Yang Jun Song Department of General Surgery The Affiliated Hospital of Xuzhou Medical UniversityXuzhou 221002China Institute of Digestive Diseases of Xuzhou Medical University Xuzhou 221002China

Chemotherapeutics are validated conventional treatments for patients with advanced cancer.However,with continual application of chemotherapeutics,Chemoresistance,which is often predictive of poor prognosis,has gradually become a concern in recent years.Circular RNAs(circ RNAs),a class of endogenous noncoding RNAs(nc RNAs)with a closed-loop structure,have been reported to be notable targets and markers for the prognosis,diagnosis,and treatment of many diseases,particularly cancer.Although dozens of studies have shown that circ RNAs play major roles in drug-resistance activity in tumors,the mechanisms by which circ RNAs affect Chemoresistance have yet to be explored.In this review,we describe the detailed mechanisms of circ RNAs and chemotherapeutics in various cancers and summarize potential therapeutic targets for drug-resistant tumors.

关键词： Circular RNA Chemoresistance drug resistance 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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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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The transcription factor ZEB1 promotes Chemoresistance in prostate cancer cell lines

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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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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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Cancerous inhibitor of protein phosphatase 2A enhances Chemoresistance of gastric cancer cells to oxaliplatin

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World Journal of Gastrointestinal Oncology 2023年第2期15卷 286-302页

作者： Yong-Xun Zhao Li-Bin Ma Ze Yang Fang Wang Hui-Ying Wang Jia-Yao Dang The Seventh Department of General Surgery The First Hospital of Lanzhou UniversityLanzhou 730000Gansu ProvinceChina Department of Pathology The First Hospital of Lanzhou UniversityLanzhou 730000Gansu ProvinceChina The First Clinical Medical School Lanzhou UniversityLanzhou 730000Gansu ProvinceChina

BACKGROUND Cancerous inhibitor of protein phosphatase 2A(CIP2A)is a newly discovered oncogene.It is an active cell proliferation regulatory factor that inhibits tumor apoptosis in gastric cancer(GC)cells.CIP2A is functionally related to Chemoresistance in various types of tumors according to recent studies.The underlying mechanism,however,is unknown.Further,the primary treatment regimen for GC is oxaliplatin-based chemotherapy.Nonetheless,it often fails due to Chemoresistance of GC cells to oxaliplatin.AIM The goal of this study was to examine CIP2A expression and its association with oxaliplatin resistance in human GC cells.METHODS Immunohistochemistry was used to examine CIP2A expression in GC tissues and adjacent normal tissues.CIP2A expression in GC cell lines was reduced using small interfering RNA.After confirming the silencing efficiency,3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide tetrazolium and flow cytometry assays were used to evaluate cell proliferation and apoptosis caused by oxaliplatin treatment.Further,the key genes and protein changes were verified using realtime quantitative reverse transcription PCR and Western blotting,respectively,before and after intervention.For bioinformatics analysis,we used the R software and Bioconductor project.For statistical analysis,we used GraphPad Prism 6.0 and the Statistical Package for the Social Sciences software version 20.0(IBM,Armonk,United States).RESULTS A high level of CIP2A expression was associated with tumor size,T stage,lymph node metastasis,Tumor Node Metastasis stage,and a poor prognosis.Further,CIP2A expression was higher in GC cells than in normal human gastric epithelial cells.Using small interfering RNA against CIP2A,we discovered that CIP2A knockdown inhibited cell proliferation and significantly increased GC cell sensitivity to oxaliplatin.Moreover,CIP2A knockdown enhanced oxaliplatin-induced apoptosis in GC cells.Hence,high CIP2A levels in GC may be a factor in Chemoresistance to oxaliplatin.In human GC cells,CIP2A regulated

关键词： Cancerous inhibitor of protein phosphatase 2A Gastric cancer Oxaliplatin Chemoresistance Akt

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XRCC1 Arg399Gln and Arg194Trp polymorphisms regulate XRCC1 expression and Chemoresistance of non-small cell lung cancer cells

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BIOCELL 2019年第3期43卷 139-144页

作者： DAIRONG LI XIANLU ZHUO LUMI HUANG XIAOHUI JI DONGLIN WANG Chongqing University Cancer Hospital&Chongqing Cancer Institute&Chongqing Cancer Hospital Chongqing400030China Postdoctoral Scientific Research Station Chongqing Cancer InstituteChongqing400030China

X-ray repair cross-complementing protein 1(XRCC1)could repair cisplatin-induced DNA damage.XRCC1 Arg399Gln and Arg194Trp variants alter XRCC1 expression and function,leading to changes in cancer sensitivity to cisplatin treatment.This study aimed to investigate the effects of XRCC1 Arg399Gln and Arg194Trp polymorphisms on cell viability,apoptosis and XRCC1 expression in cisplatin-sensitive A549 and cisplatin-resistant A549/DDP non-small cell lung cancer(NSCLC)cells.Plasmids carrying XRCC1 Arg399Gln and Arg194Trp were constructed and transfected into A549 and A549/DDP cells.RT-PCR,Western blot,MTT assay,and flow cytometry analysis were performed to assess cell viability,apoptosis,and XRCC1 expression.Compared to control cells,the viability of A549 and A549/DDP cells transfected with XRCC1 Arg399Gln and Arg194Trp was higher and the apoptosis rate was lower,and XRCC1 mRNA and protein expression levels were significantly higher.In conclusion,our results suggest that XRCC1 Arg399Gln and Arg194Trp polymorphisms change XRCC1 expression in NSCLC cells and alter the sensitivity of NSCLC to cisplatin-based chemotherapy.

关键词： Chemoresistance Non-small-cell lung cancer SNP XRCC1

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