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The Fibrillin-1/VEGFR2/STAT2 signaling axis promotes chemoresistance via modulating glycolysis and angiogenesis in ovarian cancer organoids and cells

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Cancer Communications 2022年第3期42卷 245-265页

作者： Ziliang Wang Wei Chen Ling Zuo Midie Xu Yong Wu Jiami Huang Xu Zhang Yongheng Li Jing Wang Jing Chen Husheng Wang Huizhen Sun Department of Obstetrics and Gynecology Xinhua Hospital Affiliated to Shanghai Jiaotong University School of MedicineShanghai 200092P.R.China Institute of Cancer Research and Department of Gynecology Shanghai Municipal Hospital of Traditional Chinese MedicineShanghai University of Traditional Chinese MedicineShanghai 200071P.R.China Department of Reproductive Medicine Center Zhongshan HospitalFudan UniversityShanghai 200032P.R.China Department of Pathology and Biobank Fudan University Shanghai Cancer CenterShanghai 200032P.R.China Department of Gynecological Oncology Fudan University Shanghai Cancer CenterShanghai 200032P.R.China

Background:Chemotherapy resistance is a primary reason of ovarian cancer therapy failure;hence it is important to investigate the underlying mechanisms of chemotherapy resistance and develop novel potential therapeutic targets.Methods:RNA sequencing of cisplatin-resistant and sensitive(chemoresis-tant and chemosensitive,respectively)ovarian cancer organoids was performed,followed by detection of the expression level of fibrillin-1(FBN1)in organoids and clinical specimens of ovarian cancer.Subsequently,glucose metabolism,angiogenesis,and chemosensitivity were analyzed in structural glycoprotein FBNl-knockout cisplatin-resistant ovarian cancer organoids and cell lines.To gain insights into the specific functions and mechanisms of action of FBN1 in ovarian cancer,immunoprecipitation,silver nitrate staining,mass spectrometry,immunofluorescence,Western blotting,and Forister resonance energy transfer-fluorescence lifetime imaging analyses were performed,followed by in vivo assays using vertebrate model systems of nude mice and zebrafish.Results:FBN1 expression was significantly enhanced in cisplatin-resistant ovar-ian cancer organoids and tissues,indicating that FBNI might be a key factor in chemoresistance of ovarian cancer.We also discovered that FBN1 sustained the energy stress and induced angiogenesis in vitro and in vivo,which promoted the cisplatin-resistance of ovarian cancer.Knockout of FBN1 combined with treat-ment of the antiangiogenic drug apatinib improved the cisplatin-sensitivity of ovarian cancer cells.Mechanistically,FBN1 mediated the phosphorylation of vascular endothelial growth factor receptor 2(VEGFR2)at the Tyrl054 residue,which activated its downstream focal adhesion kinase(FAK)/protein kinase B(PKB or AKT)pathway,induced the phosphorylation of signal transducer and activator of transcription 2(STAT2)at the tyrosine residue 690(Tyr690),pro-moted the nuclear translocation of STAT2,and ultimately altered the expression of genes associated with STAT2-mediated angiogenesis and glycolysis.Conclusions:T

关键词： angiogenesis chemoresistance Fibrillin-1 glycolysis organoid ovariancancer STAT2 VEGFR

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Regenerating gene 4 promotes chemoresistance of colorectal cancer by affecting lipid droplet synthesis and assembly

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世界胃肠病学杂志:英文版 2023年第35期29卷 5104-5124页

作者： Cong-Yu Zhang Rui Zhang Li Zhang Zi-Mo Wang Hong-Zhi Sun Zheng-Guo Cui Hua-Chuan Zheng Cancer Center The First Affiliated Hospital of Jinzhou Medical UniversityJinzhou 121001Liaoning ProvinceChina Department of Colorectal Surgery Liaoning Cancer HospitalShenyang 110042Liaoning ProvinceChina Department of Oncology The Affiliated Hospital of Chengde Medical UniversityChengde 067000Hebei ProvinceChina Department of Environmental Health University of Fukui School of Medical SciencesFukui 910-1193Japan

BACKGROUND Regenerating gene 4(REG4)has been proved to be carcinogenic in some cancers,but its manifestation and possible carcinogenic mechanisms in colorectal cancer(CRC)have not yet been elucidated.Our previous study found that the drug resistance of CRC cells may be closely linked to their fat metabolism.AIM To explore the role of REG4 in CRC and its association with lipid droplet formation and chemoresistance.METHODS We conducted a meta-analysis and bioinformatics and pathological analyses of REG4 expression in CRC.The effects of REG4 on the phenotypes and related protein expression were also investigated in CRC cells.We detected the impacts of REG4 on the chemoresistance and lipid droplet formation in CRC cells.Finally,we analyzed how REG4 regulated the transcription and proteasomal degradation of lipogenic enzymes in CRC cells.RESULTS Compared to normal mucosa,REG4 mRNA expression was high in CRC(Pchemoresistance not through de novo lipogenesis,but lipid droplet assembly.REG4 inhibited the transcription of acetyl-CoA carboxylase 1(ACC1)and ATP-citrate lyase(ACLY)by disassociating the complex formation of anti-acetyl(A

关键词： Colorectal cancer Regenerating gene 4 Aggressive behavior Prognosis chemoresistance Lipid droplet formation Epidermal growth factor receptor signal

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Fungal mycobiome-mediated immune response:a non-negligible promoter in pancreatic oncogenesis and chemoresistance

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Cancer Drug Resistance 2023年第2期6卷 284-290页

作者： Yaling Jiang Valentina Donati Godefridus J.Peters Elisa Giovannetti Dong Mei Deng Department of Preventive Dentistry Academic Center for Dentistry Amsterdam(ACTA)University of Amsterdam and Vrije Universiteit AmsterdamAmsterdam 1081 LANetherlands Department of Medical Oncology Amsterdam University Medical Centerslocation VUMCVrije Universiteit AmsterdamAmsterdam 1081 HVNetherlands Unit of Pathological Anatomy 2 Azienda Ospedaliero-Universitaria PisanaPisa 56100Italy Department of Biochemistry Medical University of GdanskGdansk 80-210Poland Fondazione Pisana per la Scienza ONLUS San Giuliano TermePisa 56017Italy

Pancreatic ductal adenocarcinoma(PDAC)is one of the most lethal cancers in humans due to late diagnosis and poor response to treatments.The tumor microenvironment(TME)of PDAC is characterized by a distinctive,suppressive immune profile,which inhibits the protective functions of anti-tumor immunity and thereby contributes to PDAC progression.Recently,the study of Alam et al.discovered for the first time that the intratumoral fungal mycobiome could contribute to the recruitment and activation of type 2 immune cells in the TME of PDAC via enhancing the secretion of a chemoattractant,interleukin(IL-)33.In this article,we reviewed the important findings of this study.Together with our findings,we synthetically discussed the role of the fungal mycobiome in orchestrating the immune response and thereby modulating tumor progression.

关键词： Mycobiome pancreatic cancer chemoresistance interleukin 33 type 2 immune cells

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Interaction of pregnane X receptor with hypoxiainducible factor-1 regulates chemoresistance of prostate cancer cells

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Cancer Drug Resistance 2023年第2期6卷 378-389页

作者： Jiuhui Wang Daotai Nie Department of Medical Microbiology Immunology and Cell BiologySouthern Illinois University School of MedicineSpringfieldIL 62794USA Simmons Cancer Institute Southern Illinois University School of MedicineSpringfieldIL 62794USA

Aim:The nuclear pregnane X receptor(PXR)is a pivotal regulator of steroid and xenobiotics metabolism and plays an important role in shaping tumor cell responses to chemotherapy.Hypoxia within tumor tissue has multifaceted effects,including multiple drug resistance.The goal of this study was to determine whether PXR contributes to hypoxia-induced drug resistance.Methods:Metastatic prostate cancer cells were used to study the interaction of PXR and hypoxia-inducible factor-1(HIF-1 in drug resistance associated with hypoxia.The activities of PXR and HIF-1 were determined by assays for its reporter gene or target gene expression.Co-immunoprecipitation(Co-IP)was used to determine the interaction of PXR and HIF-1.Ablation or inhibition of PXR or HIF-1 was used to determine their roles in hypoxia-induced chemoresistance.Results:PXR was activated by hypoxia,leading to increased expression of multidrug resistance protein 1(MDR1).Inhibition of PXR by pharmacological compounds or depletion by shRNAs reduced the hypoxic induction of MDR1 and sensitized prostate cancer cells to chemotherapy under hypoxia.HIF-1 was required for PXR activation under hypoxia.Co-immunoprecipitation results showed that HIF-1 and PXR could physically interact with each other,leading to crosstalk between these two transcription factors.Conclusion:PXR contributes to hypoxia-induced drug resistance in prostate cancer cells through its interaction with HIF-1.

关键词： PXR HIF-1 prostate cancer chemoresistance multidrug resistance MDR1 hypoxia

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Lysosome-mediated chemoresistance in acute myeloid leukemia

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Cancer Drug Resistance 2022年第1期5卷 233-244页

作者： Laia Cuesta-Casanovas Jennifer Delgado-Martinez Josep ***-Masana Jose M.Carbo Lise Clement-Demange Ruth M.Risueno Josep Carreras Leukaemia Research Institute(IJC) Barcelona 08916Spain Faculty of Biosciences Autonomous University of BarcelonaBellaterra(Cerdanyola del Valles)08193Spain Faculty of Pharmacy University of BarcelonaBarcelona 08028Spain Leukos Biotech Muntaner383Barcelona 08036Spain

Despite the outstanding advances in understanding the biology underlying the pathophysiology of acute myeloid leukemia(AML)and the promising preclinical data published lastly,AML treatment still relies on a classic chemotherapy regimen largely unchanged for the past five decades.Recently,new drugs have been approved for AML,but the real clinical benefit is still under evaluation.Nevertheless,primary refractory and relapse AML continue to represent the main clinical challenge,as the majority of AML patients will succumb to the disease despite achieving a complete remission during the induction phase.As such,treatments for chemoresistant AML represent an unmet need in this disease.Although great efforts have been made to decipher the biological basis for leukemogenesis,the mechanism by which AML cells become resistant to chemotherapy is largely unknown.The identification of the signaling pathways involved in resistance may lead to new combinatory therapies or new therapeutic approaches suitable for this subset of patients.Several mechanisms of chemoresistance have been identified,including drug transporters,key secondary messengers,and metabolic regulators.However,no therapeutic approach targeting chemoresistance has succeeded in clinical trials,especially due to broad secondary effects in healthy cells.Recent research has highlighted the importance of lysosomes in this phenomenon.Lysosomes’key role in resistance to chemotherapy includes the potential to sequester drugs,central metabolic signaling role,and gene expression regulation.These results provide further evidence to support the development of new therapeutic approaches that target lysosomes in AML.

关键词： Lysosome chemoresistance AML lysosomotropic drug lysosomal sequestration refractory AML

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ABTL0812 enhances antitumor effect of paclitaxel and reverts chemoresistance in triple-negative breast cancer models

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Cancer Communications 2022年第6期42卷 567-571页

作者： Emma Polonio-Alcala Sònia Solé-Sánchez Pau Munoz-Guardiola Elisabet Megías-Roda Héctor Perez-Montoyo Marc Yeste-Velasco Jose Alfón Jose Miguel Lizcano Carles Domènech Santiago Ruiz-Martínez Teresa Puig New Therapeutic Targets Laboratory(TargetsLab)-Oncology Unit Department of Medical SciencesUniversity of GironaGirona 17003Spain Product Process and Production Engineering Research Group(GREP)Department of Mechanical Engineering and Industrial ConstructionUniversity of GironaGirona 17003Spain Ability Pharmaceuticals SLCerdanyola del VallesBarcelona 08290Spain Protein Kinases and Signal Transduction Laboratory Department de Bioquimica i Biologia Molecular and Institut de NeurocienciesUniversitat Autonoma de BarcelonaBellaterraBarcelona 08193Spain

Dear Editor,Triple-negative breast cancer(TNBC)accounts for 20%of all breast carcinomas and lacks a validated targeted therapy;thus,currently,cytotoxic chemotherapy is the treatment of choice[1].Compared with other breast cancer types,patientswith TNBCare younger,have larger tumors,a higher risk of metastasis,and a higher rate of recurrence[2].Among all the subtypes described by Lehmann et al.[3],mesenchymal-like and mesenchymal stem-like(MSL)subtypes had the lowest 5-year distant metastasis-free survival rates.

关键词： ABTL0812 TRIB3 Autophagy Breast Cancer Targeted Therapy 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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Decoding Retinoblastoma: Differential Gene Expression

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International Journal of Clinical Medicine 2024年第4期15卷 177-196页

作者： Ahmed Jasim Mahmood Al-Mashhadani Franko Shehaj Lianhong Zhou Department of Ophthalmology Renmin Hospital of Wuhan University Wuhan China

Background: Retinoblastoma, the most common intraocular pediatric cancer, presents complexities in its genetic landscape that necessitate a deeper understanding for improved therapeutic interventions. This study leverages computational tools to dissect the differential gene expression profiles in retinoblastoma. Methods: Employing an in silico approach, we analyzed gene expression data from public repositories by applying rigorous statistical models, including limma and de seq 2, for identifying differentially expressed genes DEGs. Our findings were validated through cross-referencing with independent datasets and existing literature. We further employed functional annotation and pathway analysis to elucidate the biological significance of these DEGs. Results: Our computational analysis confirmed the dysregulation of key retinoblastoma-associated genes. In comparison to normal retinal tissue, RB1 exhibited a 2.5-fold increase in expression (adjusted p Conclusions: Our analysis reinforces the critical genetic alterations known in retinoblastoma and unveils new avenues for research into the disease’s molecular basis. The discovery of chemoresistance markers and immune-related genes opens potential pathways for personalized treatment strategies. The study’s outcomes emphasize the power of in silico analyses in unraveling complex cancer genomics.

关键词： Retinoblastoma Gene Expression In Silico Study Differentially Expressed Genes chemoresistance Immune Response Computational Biology

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Effect of environmental factors on chemoresistance of HepG2 cells by regulating hypoxia-inducible factor-1α

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Chinese Medical Journal 2012年第6期125卷 1095-1103页

作者： ZHU Hong LUO Shun-feng WANG Ji LI Xin WANG Hui PU Wang-yang ZHANG Hong ZHUANG Zhi-xiang Department of Oncology Second Affiliated Hospital of Soochow University Suzhou Jiangsu 215006 China Hepatic Surgery Center First Affiliated Hospital of Fujian Medical University Fuzhou Fujian 350005 China

Background Accumu1αting evidence demonstrates that the microenvironment of the host has an important effect on the chemoresistance of tumors. We also found that the formation of intrinsic multidrug resistance is re1αted to environmental factors that are common with tumor growth of hepatocellu1αr carcinoma. The aim of this study was to explore the molecu1αr mechanisms by which multidrug resistance of hepatocellu1αr carcinoma is induced by the microenvironment. In particu1αr, the regu1αtion of nuclear transcription factor （hypoxia-inducible factor-1α, HIF-1α） activation in the process of multidrug resistance formation was investigated. Methods HepG2 cells were exposed to different microenvironmental conditions respectively, such as hypoxia, stimu1αtion of glucose deprivation and transfection of p1αsmid PcDNA3/HBx. In the HepG2 cells, the expression of the re1αted MDR proteins, HIF-1α protein expression and localization, activity of extracellu1αr signal-regu1αted kinase /mitogen-activated protein kinase （ERK/MAPK） were detected. Specific inhibitor U0126 was used to block ERK/MAPK signal pathway, the alteration of HIF-1α and the re1αted MDR proteins were investigated. Multivariate analysis of variance （MANOVA） repeated measures and one-way analysis of variance （ANOVA） followed by Tukey test or t-test were used to determine differences over time and effects of the treatments. Results The above three microenvironment factors increase the expression of the re1αted MDR proteins （including P-gp, LRP, and MRP1） and induce MDR of HepG2 cells. HIF-1α was induced at the protein and mRNA levels and the nuclear translocation was also increased. The activity of ERK/MAPK was also increased in HepG2 cells. But when ERK/MAPK pathway was inhibited, the mRNA and protein decreased. Inhibition of ERK/MAPK significantly reduced HIF-1α, whereas HIF-1α mRNA levels were not affected. expression of MDR1, MRP1, and LRP was to some extent activated HIF-1α protein and the nuclear translocation of Conclusions The microenvironmental factors coul

关键词： HepG2 cells hypoxia-inducible factor-1α 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 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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