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Leptin signaling and cancer chemoresistance:Perspectives

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World Journal of Clinical Oncology 2017年第2期8卷 106-119页

作者： Pierre V Candelaria Antonio Rampoldi Adriana Harbuzariu Ruben R Gonzalez-Perez Department of Microbiology Bio-chemistry and ImmunologyMorehouse School of Medicine

Obesity is a major health problem and currently is endemic around the world. Obesity is a risk factor for several different types of cancer, significantly promoting cancer incidence, progression, poor prognosis and resistance to anti-cancer therapies. The study of this resistance is critical as development of chemoresistance is a serious drawback for the successful and effective drug-based treatments of cancer. There is increasing evidence that augmented adiposity can impact on chemotherapeutic treatment of cancer and the development of resistance to these treatments, particularly through one of its signature mediators, the adipokine leptin. Leptin is a pro-inflammatory, pro-angiogenic and pro-tumorigenic adipokine that has been implicated in many cancers promoting processes such as angiogenesis, metastasis, tumorigenesis and survival/resistance to apoptosis. Several possible mechanisms that could potentially be developed by cancer cells to elicit drug resistance have been suggested in the literature. Here, we summarize and discuss the current state of the literature on the role of obesity and leptin on chemoresistance, particularly as it relates to breast and pancreatic cancers. We focus on the role of leptin and its significance in possibly driving these proposed chemoresistance mechanisms, and examine its effects on cancer cell survival signals and expansion of the cancer stem cell sub-populations.

关键词： Obesity-related cancer Cancer stem cells Leptin chemoresistance Breast cancer Pancreatic cancer

Glioblastoma chemoresistance:roles of the mitochondrial melatonergic pathway

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Cancer Drug Resistance 2020年第3期3卷 334-355页

作者： George Anderson CRC Scotland&London Eccleston SquareLondon SW1V 1PGUK.

Treatment-resistance is common in glioblastoma(GBM)and the glioblastoma stem-like cells(GSC)from which they arise.Current treatment options are generally regarded as very poor and this arises from a poor conceptualization of the biological underpinnings of GBM/GSC and of the plasticity that these cells are capable of utilizing in response to different treatments.A number of studies indicate melatonin to have utility in the management of GBM/GSC,both per se and when adjunctive to chemotherapy.Recent work shows melatonin to be produced in mitochondria,with the mitochondrial melatonergic pathway proposed to be a crucial factor in driving the wide array of changes in intra-and inter-cellular processes,as well as receptors that can be evident in the cells of the GBM/GSC microenvironment.Variations in the enzymatic conversion of N-acetylserotonin(NAS)to melatonin may be especially important in GSC,as NAS can activate the tyrosine receptor kinase B to increase GSC survival and proliferation.Consequently,variations in the NAS/melatonin ratio may have contrasting effects on GBM/GSC survival.It is proposed that mitochondrial communication across cell types in the tumour microenvironment is strongly driven by the need to carefully control the mitochondrial melatonergic pathways across cell types,with a number of intra-and inter-cellular processes occurring as a consequence of the need to carefully regulate the NAS/melatonin ratio.This better integrates previously disparate data on GBM/GSC as well as providing clear future research and treatment options.

关键词： Glioblastoma glioblastoma stem-like cells melatonin N-acetylserotonin mitochondria metabolism circadian treatment chemoresistance tyrosine receptor kinase B

The bone marrow microenvironment as a mediator of chemoresistance in acute lymphoblastic leukemia

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Cancer Drug Resistance 2019年第4期2卷 1164-1177页

作者： Lauren K.Meyer Michelle L.Hermiston Department of Pediatrics University of CaliforniaSan FranciscoSF 94158USA

Acute lymphoblastic leukemia(ALL)is a malignancy of immature lymphoid cells that arises due to clonal expansion of cells that undergo developmental arrest and acquisition of pathogenic mutations.With the introduction of intensive multi-agent chemotherapeutic regimens,survival rates for ALL have improved dramatically over the past several decades,though survival rates for adult ALL continue to lag behind those of pediatric ALL.Resistance to chemotherapy remains a significant obstacle in the treatment of ALL,and chemoresistance due to molecular alterations within ALL cells have been described.In addition to these cell-intrinsic factors,the bone marrow microenvironment has more recently been appreciated as a cell-extrinsic mediator of chemoresistance,and it is now known that stromal cells within the bone marrow microenvironment,through direct cell-cell interactions and through the release of lymphoid-acting soluble factors,contribute to ALL pathogenesis and chemoresistance.This review discusses mechanisms of chemoresistance mediated by factors within the bone marrow microenvironment and highlights novel therapeutic strategies that have been investigated to overcome chemoresistance in this context.

关键词： Acute lymphoblastic leukemia chemotherapy chemoresistance bone marrow microenvironment

MiR-181b suppresses proliferation of and reduces chemoresistance to temozolomide in U87 glioma stem cells

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The Journal of Biomedical Research 2010年第6期24卷 436-443页

作者： Ping Li Xiaoming Lu Yingyi Wang Lihua Sun Chunfa Qian Wei Yan Ning Liu Yongping You Zhen Fu Department of Neurosurgery the First Affiliated Hospital of Nanjing Medical UniversityNanjingJiangsu 210029China Department of Neurosurgery the Affiliated Brain Hospital of Nanjing Medical UniversityNanjingJiangsu 210029China

MicroRNAs regulate self renewal and differentiation of cancer stem cells.There,we sought to identify the expression of miR-181b in glioma stem cells and investigate the biological effect of miR-181b on glioma stem cells in this study.MiR-181b expression was measured by real-time PCR in glioma stem cells isolated from U87 cells by FACS sorting.After miR-181b was overexpressed in U87 glioma stem cells by miR-181b lentiviral expression vector and/or treatment of temozolomide,secondary neurosphere assay,soft agar colony assay and MTT assay were performed.Compared with U87 cells,the expression of miR-181b was significantly decreased in U87 glioma stem cells.Overexpression of miR-181b decreased neurosphere formation by U87 glioma stem cells in vitro and suppressed colony formation in soft agar,and the cell growth inhibition rates increased in a time-dependent manner in U87 glioma stem cells infected with miR-181b lentivirus.Furthermore,miR-181b had a synergistic effect on temozolomide-induced inhibition of secondary neurosphere and soft agar colony,and on cell growth inhibition rates.MiR-181b functions as a tumor suppressor that suppresses proliferation and reduces chemoresistance to temozolomide in glioma stem cells.

关键词： miR-181b glioma stem cells proliferation chemoresistance

Sox2 enhances the tumorigenicity and chemoresistance of cancer stem-like cells derived from gastric cancer

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The Journal of Biomedical Research 2012年第5期26卷 336-345页

作者： Tian Tian Yajie Zhang Shouyu Wang Jianwei Zhou Shan Xu Department of Cell Biology Cancer Center Nanjing Medical University Nanjing Jiangsu 210029 China Department of Molecular Cell Biology & Toxicology School of Public Health Nanjing Medical University Nanjing Jiangsu 210029 China

Gastric cancer stem-like cells（GCSCs） have been identified to possess the ability of self-renewal and tumor initi-ation.However,the mechanisms involved remain largely unknown.Here,we isolated and characterized the GCSCs by side population（SP） sorting procedure and cultured sphere cells（SC） from human gastric cancer cell lines SGC-7901,BGC-823,MGC-803,HGC-27 and MKN-28.The sorting and culture assay revealed that SP cells proliferated in an asymmetric division manner.In addition,SP cells exhibited a higher potential of spheroid colony formation and greater drug resistance than non-SP cells（NSP）.Moreover,the SC were found with enhanced capabilities of drug resistance in vitro and tumorigenicity in vivo.Sox2 mRNA and protein was highly and significantly overex-pressed in the SP cells and SC.Importantly,downregulation of Sox2 with siRNA obviously reduced spheroid colony formation and doxorubicin efflux,as well as increased apoptosis rate in sphere cells in vitro and suppressed tumori-genicity in vivo.These results suggest that both SP cells and cultured SC enrich with GCSCs and that Sox2 plays a pivotal role in sustaining stem cell properties and might be a potential target for gastric cancer therapy.

关键词： side population gastric cancer stem-like cells CD44 Sox2 chemoresistance

The emerging roles of E3 ubiquitin ligases in ovarian cancer chemoresistance

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Cancer Drug Resistance 2021年第2期4卷 365-381页

作者： Yang Meng Lei Qiu Su Zhang Junhong Han Research Laboratory of Cancer Epigenetics and Genomics Department of General SurgeryFrontiers Science Center for Disease-related Molecular NetworkCancer Center and National Clinical Research Center for GeriatricsWest China HospitalSichuan UniversityChengdu 610041China

Epithelial cancer of the ovary exhibits the highest mortality rate of all gynecological malignancies in women today,since the disease is often diagnosed in advanced stages.While the treatment of cancer with specific chemical agents or drugs is the favored treatment regimen,chemotherapy resistance greatly impedes successful ovarian cancer chemotherapy.Thus,chemoresistance becomes one of the most critical clinical issues confronted when treating patients with ovarian cancer.Convincing evidence hints that dysregulation of E3 ubiquitin ligases is a key factor in the development and maintenance of ovarian cancer chemoresistance.This review outlines recent advancement in our understanding of the emerging roles of E3 ubiquitin ligases in ovarian cancer chemoresistance.We also highlight currently available inhibitors targeting E3 ligase activities and discuss their potential for clinical applications in treating chemoresistant ovarian cancer patients.

关键词： Ovarian cancer chemoresistance E3 ubiquitin ligases inhibitor

Role of cellular reprogramming and epigenetic dysregulation in acquired chemoresistance in breast cancer

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Cancer Drug Resistance 2019年第2期2卷 297-312页

作者： Logeswari Ponnusamy Prathap Kumar S.Mahalingaiah Yu-Wei Chang Kamaleshwar P.Singh Department of Environmental Toxicology The Institute of Environmental and Human Health(TIEHH)Texas Tech UniversityLubbockTexas 79409USA Metabolism and Safety ZoetisKalamazooMichigan 49007USA Preclinical Safety AbbVieNorth ChicagoIllinois 60085USA

Acquired resistance to chemotherapy is a major limitation in clinical treatment for breast cancer.Accumulating evidence from in vitro,in vivo and clinical studies suggest that acquired chemoresistance is progressive,multifactorial and involve genetic and epigenetic aberrations.Among various mechanisms that contribute to chemoresistance,cellular reprogramming has extensively been implicated in breast cancer resistance lately.Cellular reprogramming events such as acquisition of epithelial to mesenchymal transition(EMT)and cancer stemness(CSCs)not only provide cancer cells with reversible phenotypic plasticity and survival advantage against cytotoxicity but also leads to aggressiveness,metastasis,clinical resistance,tumor recurrence and poor survival.The transient and reversible nature of cellular reprogramming processes and their controlled interaction with epigenetic regulatory complexes strongly support the involvement of dynamic epigenetic regulatory network in governing the cellular reprogramming and associated acquired chemoresistance.Further,epigenetic modulations are also gaining interest as promising interventions addressing the cancer cell reprogramming machinery to overcome acquired chemoresistance.This review discusses the previous reports and our recent findings that lead to current understanding of epigenetic dysregulation dictating the cellular reprogramming processes such as acquisition of EMT and CSCs phenotype and how they co-ordinate to establish acquired drug resistance in breast cancer.

关键词： chemoresistance cellular reprogramming DNA methylation histone modifications breast cancer epithelial to mesenchymal transition cancer stem cell

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

The lncRNA BORG: a novel inducer of TNBC metastasis, chemoresistance, and disease recurrence

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Journal of Cancer Metastasis and Treatment 2019年第5期4卷 48-61页

作者： Alex J.Gooding Kimberly A.Parker Saba Valadkhan William P.Schiemann Department of Pathology Case Western Reserve UniversityClevelandOH 44106USA Department of Pharmacology Case Western Reserve UniversityClevelandOH 44106USA Department of Molecular Biology and Microbiology Case Western Reserve UniversityClevelandOH 44106USA Case Comprehensive Cancer Center Case Western Reserve UniversityClevelandOH 44106USA

Although greater than 90% of breast cancer-related mortality can be attributed to metastases, the molecular mechanisms underpinning the dissemination of primary breast tumor cells and their ability to establish malignant lesions in distant tissues remain incompletely understood. Genomic and transcriptomic analyses identified a class of transcripts called long noncoding RNA (lncRNA), which interact both directly and indirectly with key components of gene regulatory networks to alter cell proliferation, invasion, and metastasis. We identified a pro-metastatic lncRNA BMP/OP-Responsive Gene (BORG) whose aberrant expression promotes metastatic relapse by reactivating proliferative programs in dormant disseminated tumor cells (DTCs). BORG expression is broadly and strongly induced by environmental and chemotherapeutic stresses, a transcriptional response that facilitates the survival of DTCs. Transcriptomic reprogramming in response to BORG resulted in robust signaling via survival and viability pathways, as well as decreased activation of cell death pathways. As such, BORG expression acts as a (1) marker capable of predicting which breast cancer patients are predisposed to develop secondary metastatic lesions;and (2) unique therapeutic target to maximize chemosensitivity of DTCs. Here we review the molecular and cellular factors that contribute to the pathophysiological activities of BORG during its regulation of breast cancer metastasis, chemoresistance, and disease recurrence.

关键词： BORG chemoresistance disease recurrence dormancy long noncoding RNA metastasis triple-negative breast cancer