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Evaluation and simplification of risk factors in FIGO 2000 scoring system for gestational trophoblastic neoplasia:a 19-year retrospective analysis

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Journal of Zhejiang University-Science B(Biomedicine & Biotechnology) 2022年第3期23卷 218-229页

作者： Yang WENG Yuanyuan LIU Chitapa BENJOED Xiaodong WU Sangsang TANG Xiao LI Xing XIE Weiguo LU Women’s Reproductive Health Key Research Laboratory of Zhejiang Province Women’s HospitalSchool of MedicineZhejiang UniversityHangzhou310006China Department of Gynecologic Oncology Women’s HospitalSchool of MedicineZhejiang UniversityHangzhou310006China Center for Uterine Cancer Diagnosis and Therapy Research of Zhejiang Province Hangzhou310006China Cancer Center of Zhejiang University Hangzhou310058China

Objective The International Federation of Gynecology and Obstetrics(FIGO)2000 scoring system classifies gestational trophoblastic neoplasia(GTN)patients into low-and high-risk groups,so that single-or multi-agent chemotherapy can be administered accordingly.However,a number of FIGO-defined low-risk patients still exhibit resistance to single-agent regimens,and the risk factors currently adopted in the FIGO scoring system possess inequable values for predicting single-agent chemoresistance.The purpose of this study is therefore to evaluate the efficacy of risk factors in predicting single-agent chemoresistance and explore the feasibility of simplifying the FIGO 2000 scoring system for GTN.Methods The clinical data of 578 GTN patients who received chemotherapy between January 2000 and December 2018 were retrospectively reviewed.Univariate and multivariate logistic regression analyses were carried out to identify risk factors associated with single-agent chemoresistance in low-risk GTN patients.Then,simplified models were built and compared with the original FIGO 2000 scoring system.Results Among the eight FIGO risk factors,the univariate and multivariate analyses identified that pretreatment serum human chorionic gonadotropin(hCG)level and interval from antecedent pregnancy were consistently independent predictors for both first-line and subsequent single-agent chemoresistance.The simplified model with two independent factors showed a better performance in predicting single-agent chemoresistance than the model with the other four non-independent factors.However,the addition of other co-factors did improve the efficiency.Overall,simplified models can achieve favorable performance,but the original FIGO 2000 prognostic system still features the highest discrimination.Conclusions Pretreatment serum hCG level and interval from antecedent pregnancy were independent predictors for both first-line and subsequent single-agent chemoresistance,and they had greater weight than other non-independent factors in predicting single

关键词： Gestational trophoblastic neoplasia(GTN) Single-agent chemotherapy chemoresistance Risk factor

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Expert opinion on translational research for advanced glioblastoma treatment

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Cancer Biology & Medicine 2023年第5期20卷 344-352页

作者： Xiaoteng Cui Yunfei Wang Junhu Zhou Qixue Wang Chunsheng Kang Laboratory of Neuro-oncology Tianjin Neurological InstituteKey Laboratory of Post-Neuro Injury Neuro-Repair and Regeneration in Central Nervous SystemMinistry of Education and Tianjin CityTianjin Medical University General HospitalTianjin 300052China

Malignant gliomas are known to be one of the most difficult diseases to diagnose and treat because of the infiltrative growth pattern,rapid progression,and poor prognosis.Many antitumor drugs are not ideal for the treatment of gliomas due to the blood-brain barrier.Temozolomide(TMZ)is a DNA alkylating agent that can cross the blood-brain barrier.As the only first-line chemotherapeutic drug for malignant gliomas at present,TMZ is widely utilized to provide a survival benefit;however,some patients are inherently insensitive to TMZ.In addition,patients could develop acquired resistance during TMZ treatment,which limits antitumor efficacy.To clarify the mechanism underlying TMZ resistance,numerous studies have provided multilevel solutions,such as improving the effective concentration of TMZ in tumors and developing novel small molecule drugs.This review discusses the in-depth mechanisms underlying TMZ drug resistance,thus aiming to provide possibilities for the establishment of personalized therapeutic strategies against malignant gliomas and the accelerated development and transformation of new targeted drugs.

关键词： Malignant gliomas glioblastoma temozolomide chemoresistance small molecule drugs

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Ascochlorin overcomes chemoresistance and regulates the plasticity of doxorubicin induced EMT via modulation of the NF-кB pathway in hepatocellular carcinoma

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中国药理学与毒理学杂志 2015年第S1期29卷 79-80页

作者： Xiao-yunDAI KwangSeokAHN ChulwonKIM MuthuKSHANMUGAM FengLI Ji-zhongSHI AlanPremKUMAR Ling-zhiWANG BoonCherGOH JunjiMAGAE TinaHONG KamMHUI GautamSETHI Department of Pharmacology Yong Loo Lin School of Medicine National University of Singapore Singapore 117597 College of Oriental Medicine Kyung Hee University Seoul 130-701 Republic of Korea Cancer Science Institute of Singapore Cancer Science Singapore 117599 Department of Haematology-Oncology National University Health System Singapore 117599 Magae Bioscience Institute 49-4 Fujimidai Tsukuba 300-1263 Japan Division of Cellular and Molecular Research Humphrey Oei Institute of Cancer Research National Cancer Centre Singapore 169610

OBJECTIVE Doxorubicin-based therapy has been found to be not significantly effective for the treatment of advanced stage hepatocellular carcinomas(HCCs),which often undergo epithelial-mesenchymal transition(EMT)during tumor progression.Increasing evidence suggest(s)that epithelial cell transformation to mesenchymal state canenhance the ability to self-renew and confer greater resistance to the conventional chemotherapeutic drugs.The aim of this study was to examine the potential efficacyof ascochlorin,an isoprenoid antibiotic to overcome drug resistance induced by doxorubicin in HCC cell lines and to elucidate its underlying mechanism(s)of action.METHODS The effect of doxorubicin and ascochlorin on HCC cell lines was determined by MTT,Western blotting,immunofluorescence and NF-кB DNA binding assays.RESULTS Our results indicate that HCC cells that show a mesenchymal-like phenotype,are resistance to the doxorubicin therapy which directly correlated with an increased slug expression.We also observed that activation of NF-кB pathway plays an essential role in doxorubicin induced-chemoresistance and pharmacological inhibition of this pathway with ascochlorin can significantly reverse drug-induced invasion/migration and resistance in HCC cells.CONCLUSION Our results indicate that combination treatment of doxorubicin with ascochlorin has the potential to inhibit HCC growth and metastasis.

关键词： doxorubicin ascochlorin chemoresistance EMT NF-кB

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Emerging roles of Aurora-A kinase in cancer therapy resistance

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药学学报:英文版 2023年第7期13卷 2826-2843页

作者： Dayong Zheng Jun Li Han Yan Gang Zhang Wei Li Edward Chu Ning Wei School of Pharmacy North China University of Science and TechnologyTangshan 063210China Basic Medical Science College Liaoning University of Traditional Chinese MedicineShenyang 110032China Division of Biology and Biological Engineering California Institute of TechnologyPasadenaCA 91125USA Department of Oncology and Cancer Therapeutics Program Montefiore Einstein Cancer CenterAlbert Einstein College of MedicineBronxNY 10461USA

Aurora kinase A(Aurora-A),a serine/threonine kinase,plays a pivotal role in various cellular processes,including mitotic entry,centrosome maturation and spindle formation.Overexpression or gene-amplification/mutation of Aurora-A kinase occurs in different types of cancer,including lung cancer,colorectal cancer,and breast cancer.Alteration of Aurora-A impacts multiple cancer hallmarks,especially,immortalization,energy metabolism,immune escape and cell death resistance which are involved in cancer progression and resistance.This review highlights the most recent advances in the oncogenic roles and related multiple cancer hallmarks of Aurora-A kinase-driving cancer therapy resistance,including chemoresistance(taxanes,cisplatin,cyclophosphamide),targeted therapy resistance(osimertinib,imatinib,sorafenib,etc.),endocrine therapy resistance(tamoxifen,fulvestrant) and radioresistance.Specifically,the mechanisms of Aurora-A kinase promote acquired resistance through modulating DNA damage repair,feedback activation bypass pathways,resistance to apoptosis,necroptosis and autophagy,metastasis,and stemness.Noticeably,our review also summarizes the promising synthetic lethality strategy for Aurora-A inhibitors in RB1,ARID1A and MYC gene mutation tumors,and potential synergistic strategy for m TOR,PAK1,MDM2,MEK inhibitors or PD-L1 antibodies combined with targeting Aurora-A kinase.In addition,we discuss the design and development of the novel class of Aurora-A inhibitors in precision medicine for cancer treatment.

关键词： Aurora-A Therapy resistance chemoresistance Targeted therapy Radioresistance Synthetic lethality Alisertib PROTAC

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Shear Stress Regulates Tumor Cell Mechanics and Actomyosin-Dependent Survival and chemoresistance

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医用生物力学 2019年第A1期34卷 142-143页

作者： Ying XIN Junfan WANG Kai TANG Youhua TAN HongKong Polytechnic University Department Of Biomedical EngineeringHong KongChina The Hong KongPolytechnic University Shenzhen Research Institute ShenzhenChina

Metastasis is the main cause of cancer death,and tumor cells mainly disseminate to the distal organs through the blood circulation,in which they experience considerable levels of fluid shear stress.CTCs are heterogeneous with diverse subpopulations of distinct genotypes and phenotypes and the frequency of CTCs is correlated with poor prognosis and overall survival in cancer patients.Less than 0.01%of them may eventually generate metastatic tumors in secondary sites,indicating the inefficiency of metastasis.Nevertheless,metastasis accounts for over 90%of cancer-related deaths,suggesting that a subpopulation of CTCs are able to survive the metastatic process and form metastases.To target metastasis,it is thus essential to understand the roles of various factors during dissemination in the survival and functions of CTCs.However,the effects of hemodynamic shear stress on biophysical properties and functions of CTCs in suspension are not fully understood.This study was to investigate the effect of hemodynamic shear stress on the survival and anti-chemotherapy ability of suspended circulating tumor cells during metastasis,and the effect of actomyosin activity on this regulation.In this study,we developed a circulatory system to generate physiologic levels of hemodynamic shear stress,which mimicked certain important aspects of the CTC microenvironment in blood circulation.The survival of tumor cells in suspension,as a model for real CTCs,under different shear stress and circulation duration was examined.We found that the majority of breast tumor cells s in suspension can be eliminated by hemodynamic shear stress.The surviving cells exhibit unique biophysical properties,including significantly retarded cell adhesion,mesenchymal-like cell morphology,and reduced F-actin expression and cellular stiffness.Cancer stem cells which has been reported in other papers have lower stiffness compared with conventional tumor cells showed significantly higher survival in blood flow.Importantly,low actomyosin activity promotes the survi

关键词： Tumor Cell Mechanics Actomyosin-Dependent Survival chemoresistance

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A targetable pathway to eliminate TRA-1-60^(+)/TRA-1-81^(+)chemoresistant cancer cells

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Journal of Molecular Cell Biology 2023年第6期15卷 25-39页

作者： Lei Tan Xiaohua Duan Pratyusha Mutyala Ting Zhou Sadaf Amin Tuo Zhang Brian Herbst Gokce Askan Tomer Itkin Zhaoying Xiang Fabrizio Michelassi Michael D.Lieberman Christine AIacobuzio-Donahue Steven DLeach Todd Evans Shuibing Chen Department of Surgery Weill Cornell MedicineNew YorkNY 10065USA Center for Energy Metabolism and Reproduction Institute of Biomedicine and BiotechnologyShenzhen Institute of Advanced TechnologyChinese Academy of SciencesShenzhen 518055China Center for Genomic Health Weill Cornell MedicineNew YorkNY 10065USA The SKI Stem Cell Research Facility The Center for Stem Cell Biology and Developmental Biology ProgramMemorial Sloan Kettering Cancer CenterNew YorkNY 10065USA Genomic Resource Core Facility Weill Cornell Medical CollegeNew YorkNY 10065USA Rubenstein Center for Pancreatic Cancer Research Memorial Sloan Kettering Cancer CenterNew YorkNY 10065USA Division of Regenerative Medicine Hartman Institute for Therapeutic Organ RegenerationAnsary Stem Cell InstituteDepartment of MedicineWeill Cornell MedicineNew YorkNY 10065USA Dartmouth Cancer Center Darmouth CollegeHanoverNH 03755USA

chemoresistance is a primary cause of treatment failure in pancreatic cancer.Identifying cell surface markers specifically expressed in chemoresistant cancer cells(CCCs)could facilitate targeted therapies to overcome chemoresistance.We performed an antibody-based screen and found that TRA-1-60 and TRA-1-81,two‘stemness’cell surface markers,are highly enriched in CCCs.Further-more,TRA-1-60^(+)/TRA-1-81^(+)cells are chemoresistant compared to TRA-1-60^(-)/TRA-1-81^(-)cells.Transcriptome profiling identified UGT1A10,shown to be both necessary and sufficient to maintain TRA-1-60/TRA-1-81 expression and chemoresistance.From a high-content chemical screen,we identified Cymarin,which downregulates UGT1A10,eliminates TRA-1-60/TRA-1-81 expression,and increases chemosensitivity both in vitro and in vivo.Finally,TRA-1-60/TRA-1-81 expression is highly specific in primary cancer tissue and positively correlated with chemoresistance and short survival,which highlights their potentiality for targeted therapy.Therefore,we discovered a novel CCC surface marker regulated by a pathway that promotes chemoresistance,as well as a leading drug candidate to target this pathway.

关键词： pancreatic cancer TRA-1-60/TRA-1-81 chemoresistance UGT1A10 Cymarin

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Leptin-induced Notch and IL-1 signaling crosstalk in endometrial adenocarcinoma is associated with invasiveness and chemoresistance

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World Journal of Clinical Oncology 2019年第6期10卷 222-233页

作者： Danielle Daley-Brown Adriana Harbuzariu Ann Anu Kurian Gabriela Oprea-Ilies Ruben Rene Gonzalez-Perez Department of Microbiology Biochemistry and Immunology Morehouse School of Medicine Atlanta GA 30310 United States Department of Pathology and Laboratory Medicine Emory University Atlanta GA 30322 United States

BACKGROUND Obesity is a recognized risk factor for endometrial cancer (EmCa) and other cancer types. Leptin levels are significantly increased in obese individuals. Leptin-induced signaling crosstalk [Notch, Interleukin-1 (IL-1) and leptin outcome, NILCO] has been associated with breast cancer progression. This complex signaling crosstalk affects cancer cell proliferation, migration, invasion, angiogenesis, apoptosis and chemoresistance. NILCO expression was previously detected in human EmCa. However, it is unknown whether leptin regulates NILCO and alters EmCa’s response to chemotherapeutics. It is hypothesized that leptin induces NILCO and increases aggressiveness and chemoresistance in EmCa cells. AIM To determine whether leptin induces NILCO molecules in EmCa affecting cell proliferation, aggressiveness and chemoresistance. METHODS Leptin’s effects on the expression of NILCO molecules [mRNAs and proteins for Notch receptors (Notch1-4), ligands (JAG1 and DLL4) and downstream effectors (survivin, Hey2), and leptin (OB-R) and IL-1 (IL-1R tI) receptors] was examined in EmCa cells (type I: Ishikawa, and HEC-1A, and type II: An3Ca and KLE) using Real-time PCR and Western blot analysis, respectively. In addition, the effects of leptin on cell cycle, proliferation and cell invasion were determined using cytometric analysis (Cellometer Vision CBA system), MTT cell proliferation and Matrigel-based invasion assays, respectively. Inhibitors of leptin (nanoparticlebound leptin peptide receptor antagonist-2, IONP-LPrA2), IL-1 (anti-IL-1R tI antibody) and Notch (siRNA interference RNA) were used to investigate NILCO’s effects on cell proliferation and invasion. Leptin’s effects on Paclitaxel cytotoxicity in EmCa cells was determined by the CCK8 and Cellometer-based Annexin V assays. RESULTS For the first time it was shown that leptin is an inducer of Notch in EmCa. Experimental data suggest that leptin induced the expression of NILCO molecules, promoted proliferation and S- phase progression, and reduced Paclitaxel cytotoxi

关键词： Endometrial cancer Leptin Notch Interleukin-1 Notch, IL-1 and Leptin crosstalk outcome chemoresistance

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MicroRNAs contribute to ATP-binding cassette transporter-and autophagy-mediated chemoresistance in hepatocellular carcinoma

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World Journal of Hepatology 2019年第4期11卷 344-358页

作者： María V Espelt María L Bacigalupo Pablo Carabias María F Troncoso Facultad de Farmacia y Bioquímica Instituto de Química y Fisicoquímica Biológicas Consejo Nacional de Investigaciones Científicas y Técnicas Universidad de Buenos Aires

Hepatocellular carcinoma(HCC) has an elevated mortality rate, largely because of high recurrence and metastasis. Additionally, the main obstacle during treatment of HCC is that patients usually develop resistance to chemotherapy.Cancer drug resistance involves many different mechanisms, including alterations in drug metabolism and processing, impairment of the apoptotic machine, activation of cell survival signaling, decreased drug sensitivity and autophagy, among others. Nowadays, miRNAs are emerging as master regulators of normal physiology-and tumor-related gene expression. In HCC,aberrant expression of many miRNAs leads to chemoresistance. Herein, we particularly analyzed miRNA impact on HCC resistance to drug therapy. Certain miRNAs target ABC(ATP-binding cassette) transporter genes. As most of these miRNAs are downregulated in HCC, transporter levels increase and intracellular drug accumulation decrease, turning cells less sensitive to death. Others miRNAs target autophagy-related gene expression, inhibiting autophagy and acting as tumor suppressors. Nevertheless, due to its downregulation in HCC, these miRNAs do not inhibit autophagy or tumor growth and, resistance is favored.Concluding, modulation of ABC transporter and/or autophagy-related gene expression or function by miRNAs could be determinant for HCC cell survival under chemotherapeutic drug treatment. Undoubtedly, more insights on the biological processes, signaling pathways and/or molecular mechanisms regulated by miRNAs are needed. Anyway, miRNA-based therapy together with conventional chemotherapeutic drugs has a great future in cancer therapy.

关键词： Hepatocellular carcinoma chemoresistance ABC transporter Autophagy miRNA

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Concurrent silencing of TBCE and drug delivery to overcome platinum-based resistance in liver cancer

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Acta Pharmaceutica Sinica B 2023年第3期13卷 967-981页

作者： Senlin Li Siyu Chen Zhihui Dong Xingdong Song Xiuling Li Ziqi Huang Huiru Li Linzhuo Huang Ganyuan Zhuang Ran Lan Mingyan Guo Wende Li Phei Er Saw Lei Zhang Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation Guangdong-Hong Kong Joint Laboratory for RNA MedicineSun Yat-sen Memorial HospitalSun Yat-sen UniversityGuangzhou510120China Department of Hepatobiliary Surgery Sun Yat-sen Memorial HospitalSun Yat-sen UniversityGuangzhou 510120China Guangdong Laboratory Animals Monitoring Institute Guangdong Key Laboratory of Laboratory AnimalsGuangzhou510663China Department of Anesthesiology Sun Yat-sen Memorial HospitalSun Yat-sen UniversityGuangzhou510120China

Platinum-based chemotherapy resistance is a key factor of poor prognosis and recurrence in hepatocellular carcinoma(HCC).Herein,RNAseq analysis revealed that elevated tubulin folding cofactor E(TBCE)expression is associated with platinum-based chemotherapy resistance.High expression of TBCE contributes to worse prognoses and earlier recurrence among liver cancer patients.Mechanistically,TBCE silencing significantly affects cytoskeleton rearrangement,which in turn increases cisplatin-induced cycle arrest and apoptosis.To develop these findings into potential therapeutic drugs,endosomal pH-responsive nanoparticles(NPs)were developed to simultaneously encapsulate TBCE siRNA and cisplatin(DDP)to reverse this phenomena.NPs(siTBCE+DDP)concurrently silenced TBCE expression,increased cell sensitivity to platinum treatment,and subsequently resulted in superior anti-tumor effects both in vitro and in vivo in orthotopic and patient-derived xenograft(PDX)models.Taken together,NP-mediated delivery and the co-treatment of siTBCE+DDP proved to be effective in reversing chemotherapy resistance of DDP in multiple tumor models.

关键词： Hepatocellular carcinoma Tubulin folding cofactor E chemoresistance siRNA delivery RNA interference Nanoparticle Combination therapy Nanomedicine

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GDF15 negatively regulates chemosensitivity via TGFBR2-AKT pathway-dependent metabolism in esophageal squamous cell carcinoma

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Frontiers of Medicine 2023年第1期17卷 119-131页

作者： Yingxi Du Yarui Ma Qing Zhu Yong Fu Yutong Li Ying Zhang Mo Li Feiyue Feng Peng Yuan Xiaobing Wang State Key Laboratory of Molecular Oncology National Cancer Center/National Clinical Research Center for Cancer/Cancer HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100021China Department of Clinical Laboratory Beijing Friendship HospitalCapital Medical UniversityBeijing 100050China Township Health Center in Tanggou Town Wuhu 24100China Thoracic Surgery Department National Cancer Center/National Clinical Research Center for Cancer/Cancer HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100021China Department of VIP Medical Services National Cancer Center/National Clinical Research Center for Cancer/Cancer HospitalChinese Academy of Medical Sciences and Peking Union Medical CollegeBeijing 100021China

Treating patients with esophageal squamous cell carcinoma(ESCC)is challenging due to the high chemoresistance.Growth differentiation factor 15(GDF15)is crucial in the development of various types of tumors and negatively related to the prognosis of ESCC patients according to our previous research.In this study,the link between GDF15 and chemotherapy resistance in ESCC was further explored.The relationship between GDF15 and the chemotherapy response was investigated through in vitro and in vivo studies.ESCC patients with high levels of GDF15 expression showed an inferior chemotherapeutic response.GDF15 improved the tolerance of ESCC cell lines to low-dose cisplatin by regulating AKT phosphorylation via TGFBR2.Through an in vivo study,we further validated that the anti-GDF15 antibody improved the tumor inhibition effect of cisplatin.Metabolomics showed that GDF15 could alter cellular metabolism and enhance the expression of UGT1A.AKT and TGFBR2 inhibition resulted in the reversal of the GDF15-induced expression of UGT1A,indicating that TGFBR2-AKT pathway-dependent metabolic pathways were involved in the resistance of ESCC cells to cisplatin.The present investigation suggests that a high level of GDF15 expression leads to ESCC chemoresistance and that GDF15 can be targeted during chemotherapy,resulting in beneficial therapeutic outcomes.

关键词： GDF15 esophageal squamous cell carcinoma chemoresistance cellular metabolism TGFBR2 AKT

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