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Poorly controlled type Ⅱ diabetes mellitus significantly enhances postoperative chemoresistance in patients with stage Ⅲ colon cancer

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World Journal of Gastroenterology 2025年第3期31卷 29-41页

作者： Ruo-Yu Guan Jia-Wei Wu Zi-Yun Yuan Zhi-Yuan Liu Zi-Zhu Liu Zhi-Cong Xiao Jing-Hui Li Cheng-Zhi Huang Jun-Jiang Wang Xue-Qing Yao Guangdong Cardiovascular Institute Guangdong Provincial People’s HospitalGuangdong Academy of Medical SciencesSouthern Medical UniversityGuangzhou 510080Guangdong ProvinceChina Department of Gastrointestinal Surgery Department of General SurgeryGuangdong Provincial People’s Hospital(Guangdong Academy of Medical Sciences)Southern Medical UniversityGuangzhou 510080Guangdong ProvinceChina Department of General Surgery Guangdong Provincial People’s Hospital Ganzhou Hospital(Ganzhou Municipal Hospital)Ganzhou 341000Jiangxi ProvinceChina Shantou University Medical College Shantou 515041Guangdong ProvinceChina School of Medicine South China University of TechnologyGuangzhou 510006Guangdong ProvinceChina Gannan Medical University Ganzhou 341000Jiangxi ProvinceChina

BACKGROUND Type Ⅱ diabetes mellitus(T2DM)has been associated with increased risk of colon cancer(CC)and worse prognosis in patients with *** effects of T2DM on postoperative chemoresistance rate(CRR)and long-term disease-free survival(DFS)and overall survival(OS)in patients with stage Ⅲ CC who receive curative resection remain *** To investigate whether T2DM or glycemic control is associated with worse postoperative survival outcomes in stage Ⅲ *** This retrospective cohort study included 278 patients aged 40-75 years who underwent surgery for stage Ⅲ CC from 2018 to *** on preoperative T2DM history,the patients were categorized into non-DM(n=160)and DM groups(n=118).The latter was further divided into well-controlled(n=73)and poorly controlled(n=45)groups depending on the status of glycemic ***,OS,and CRR were compared between the groups and Cox regression analysis was used to identify risk *** Patients in the DM and non-DM groups demonstrated similar DFS,OS,and CRR(DFS:72.03%vs 78.75%,P=0.178;OS:81.36%vs 83.12%,P=0.638;CRR:14.41%vs 7.5%,P=0.063).Poorly controlled DM was associated with a significantly worse prognosis and higher CRR than well-controlled DM(DFS:62.22%vs 78.07%,P=0.021;OS:71.11%vs 87.67%,P=0.011;CRR:24.40%vs 8.22%,P=0.015).High preoperative fasting plasma glucose[DFS:Hazard ratio(HR)=2.684,P<0.001;OS:HR=2.105,P=0.019;CRR:HR=2.214,P=0.005]and glycosylated hemoglobin levels(DFS:HR=2.344,P=0.006;OS:HR=2.119,P=0.021;CRR:HR=2.449,P=0.009)indicated significantly poor prognosis and high CRR,while T2DM history did not(DFS:HR=1.178,P=0.327;OS:HR=0.933,P=0.739;CRR:HR=0.997,P=0.581).CONCLUSION Increased preoperative fasting plasma glucose and glycosylated hemoglobin levels,but not T2DM history,were identified as risk factors associated with poor postoperative outcomes and high CRR in patients with stage Ⅲ CC.

关键词： Colon cancer chemoresistance Diabetes mellitus Prognosis TypeⅡdiabetes mellitus

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Mechanistic link between long noncoding RNA and stability of oncogene reveals stemness and chemoresistance of hepatocellular carcinoma

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World Journal of Gastroenterology 2025年第7期31卷 160-162页

作者： Yu-Bo Liang Xing-Ming Chen Wan-Ling Luo Yang Ke Department of Hepatobiliary Surgery The Second Affiliated Hospital of Kunming Medical UniversityKunming 650101Yunnan ProvinceChina Department of Hepatobiliary Surgery and Department of Surgical Education and Research The Second Affiliated Hospital of Kunming Medical UniversityKunming 650101Yunnan ProvinceChina

This letter comments on the recently published manuscript by Yu et al,in which the authors revealed a novel mechanism by which the m6A-modified long noncoding RNA kinesin family member 9-antisense RNA 1 promotes stemness and sorafenib resistance of hepatocellular carcinoma(HCC)through ubiquitinspecific peptidase 1-mediated deubiquitination of oncogene short stature homeobox *** the high mortality rate and poor prognosis of HCC,the findings by Yu et al open a new avenue for overcoming HCC burden by focusing on kinesin family member 9-antisense RNA 1 and short stature homeobox 2 as prognostic markers and therapeutic targets.

关键词： Kinesin family member 9-antisense RNA 1 Hepatocellular carcinoma Ubiquitin-specific peptidase 1 Short stature homeobox 2 chemoresistance

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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 ***,with continual application of chemotherapeutics,chemoresistance,which is often predictive of poor prognosis,has gradually become a concern in recent *** 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 *** 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 *** 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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Akt isoforms differentially provide for chemoresistance in prostate cancer

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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 *** 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 ***,we characterized Akt isoform expressions in primary and metastatic prostate cancers,as well as their individual contributions to ***:Akt isoforms and E-cadherin were manipulated with drugs,knocked down,and over *** cell killing was determined in vitro and in *** survival was calculated from patient records and ***:Pan-Akt inhibition sensitized tumor cells to chemotherapy,and specific blockade of Akt1 or/and Akt2 caused cells to be more *** 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 *** human specimens,we found Akt1 and Akt2 positively correlated,whereas Akt3 inversely correlated,with the overall survival of prostate cancer ***1high/Akt2high/Akt3low tumors had the worst ***:E-cadherin-induced activation of Akt1/2 isoforms was the essential mechanism of chemoresistance,whereas Akt3 made cells more *** 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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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 *** 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 *** mechanisms involved in this protective effect are still *** a previous work,we demonstrated that ZEB1 expression induced an EMT-like phenotype in prostate cancer cell *** this work,we used prostate cancer cell lines 22Rvl and DU145 to study the effect of ZEB1 modulation on docetaxel resistance and its possible *** results showed that ZEB1 overexpression conferred to 22Rvl cell resistance to docetaxel while its silencing made DU145 cells more sensitive to *** 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 ***4 inhibition,using MK571,resensitized cells with ZEB1 overexpression to docetaxel *** 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 *** response to docetaxel in our model seems to be mediated mainly by activation of the apoptotic death *** 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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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 *** the current study,we determined the relevant players and role of N^(6)-methyladenine(m^(6)A)RNA methylation in cervical cancer ***:The roles of m^(6)A RNA methylation and centromere protein K(CENPK)in cervical cancer were analyzed using bioinformatics *** RNA immunoprecipitation was adopted to detect m^(6)A modification of CENPK *** cervical cancer clinical samples,cell lines,and xenografts were used for analyzing gene expression and *** 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,*** blot analysis,co-immunoprecipitation,chromatin immunoprecipitation,and luciferase reporter,cycloheximide chase,and cell fractionation assays were performed to elucidate the underlying ***: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 *** 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 *** dysregulation ultimately enhanced the tumorigenic pathways required for cell stemness,DNA damage repair pathways necessary f

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

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*** of *** 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 *** emerging evidence indicates that the epithelial-to-mesenchymal transition(EMT)may play pivotal roles in the development of chemoresistance and *** a hallmark of EMT,E-cadherin is suggested to be a key marker in the development of ***,the molecular mechanisms underlying PCa chemoresistance remain *** 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 ***:Parental PC3 and DU145 cells and their chemoresistant PC3-Tx R and DU145-Tx R cells were ***3-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 *** of EMT phenotype-related markers and signaling pathways were assessed by Western blotting and quantitative real-time polymerase chain *** cell migration,invasion,and colony formation were then evaluated by wound healing,transwell,and colony formation assays,*** drug sensitivity was evaluated using MTS ***: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 *** 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 *** particular,the sensitivity to paclitaxel was reactivated in E-cadherin-overexpressing PC3-Tx R and DU145-Tx R *** E-cadherin expression was silenced in parental PC3 and DU145 cells,the expression of Vimentin and Snail was up-regulated,and,pa

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

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N6-methyladenosine reader hnRNPA2B1 recognizes and stabilizes NEAT1 to confer chemoresistance in gastric cancer

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Cancer Communications 2024年第4期44卷 469-490页

作者： Jiayao Wang Jiehao Zhang Hao Liu Lingnan Meng Xianchun Gao Yihan Zhao Chen Wang Xiaoliang Gao Ahui Fan Tianyu Cao Daiming Fan Xiaodi Zhao Yuanyuan Lu State Key Laboratory of Holistic Integrative Management of Gastrointestinal Cancers and National Clinical Research Center for Digestive Diseases Xijing Hospital of Digestive DiseasesFourth Military Medical UniversityXi’anShaanxiP.R.China The Air Force Hospital of Southern Theater Command GuangzhouGuangdongP.R.China National Center for International Research of Bio-targeting Theranostics Guangxi Key Laboratory of Bio-targeting TheranosticsGuangxi Medical UniversityNanningGuangxiP.R.China Second Clinical College Shaanxi University of Traditional Chinese MedicineXianyangShaanxiP.R.China College of Life Sciences Northwest UniversityXi’anShaanxiP.R.China

Background:chemoresistance is a major cause of treatment failure in gas-tric cancer(GC).Heterogeneous nuclear ribonucleoprotein A2B1(hnRNPA2B1)is an N6-methyladenosine(m^(6)A)-binding protein involved in a variety of ***,whether m^(6)A modification and hnRNPA2B1 play a role in GC chemoresistance is largely *** this study,we aimed to investigate the role of hnRNPA2B1 and the downstream mechanism in GC ***:The expression of hnRNPA2B1 among public datasets were analyzed and validated by quantitative PCR(qPCR),Western blotting,immunoflu-orescence,and immunohistochemical *** biological functions of hnRNPA2B1 in GC chemoresistance were investigated both in vitro and in *** sequencing,methylated RNA immunoprecipitation,RNA immunoprecipi-tation,and RNA stability assay were performed to assess the association between hnRNPA2B1 and the binding *** role of hnRNPA2B1 in maintenance of GC stemness was evaluated by bioinformatic analysis,qPCR,Western blotting,immunofluorescence,and sphere formation *** expression patterns of hnRNPA2B1 and downstream regulators in GC specimens from patients who received adjuvant chemotherapy were analyzed by RNAscope and multiplex ***:Elevated expression of hnRNPA2B1 was found in GC cells and tis-sues,especially in multidrug-resistant(MDR)GC cell *** expression of hnRNPA2B1 was associated with poor outcomes of GC patients,especially in those who received 5-fluorouracil *** hnRNPA2B1 effectively sensitized GC cells to chemotherapy by inhibiting cell proliferation and induc-ing apoptosis both in vitro and in ***,hnRNPA2B1 interacted with and stabilized long noncoding RNA NEAT1 in an m^(6)A-dependent ***,hnRNPA2B1 and NEAT1 worked together to enhance the stemness properties of GC cells via Wnt/β-catenin signaling *** clin-ical specimens from GC patients subjected to chemotherapy,the expression levels of

关键词： chemoresistance gastric cancer hnRNPA2B1 NEAT1 stemness

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

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Journal of Molecular Cell Biology 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 *** 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 *** report another aspect of the interplay between p53 and *** 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 *** 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 *** studies suggest that elevated Smad1 and momentary activation inhibit cell proliferation by upregulating p57Kip2 and enhancing Atm–Chk2 ***,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 *** 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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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 *** association of hepatitis B virus(HBV)infection with HCC is hitherto *** miRNAs contribute to cancer progression and *** X protein has been known to modulate miRNAs that facilitate cell proliferation and the process of ***,there has been no report on hepatitis B core antigen(HBc)regulating exosomal miRNAs to induce drug resistance of HCC *** To elucidate the mechanism by which HBc promotes Doxorubicin hydrochloride(Dox)resistance in *** Exosomes were isolated by *** 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)*** level of miR-135a-5p in patient tissue samples was detected by quantitative polymerase chain *** and luciferase assay were used to predict and prove the target gene of ***,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 *** We found that HBc increased the expression of exosomal *** analysis of bioinformatics and patient samples found that miR-135a-5p was increased in HCC tissues in comparison with paracancerous *** analysis and in vitro validation identified vesicle-associated membrane protein 2(VAMP2)as a novel target gene of *** assays showed that exosomal miR-135a-5p induced apoptosis protection,cell proliferation,and chemotherapy resistance in *** addition,the rescue experiment demonstrated that VAMP2 reversed apoptosis protection,cell growth,and drug resistance by ***,HBc promoted HCC anti-apoptosis,proliferation,and drug resistance and prevented Dox-i

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

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