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SOX transcription factors and glioma stem cells:Choosing between stemness and differentiation

World Journal of Stem Cells 2021年第10期13卷 1417-1445页

作者： Milena Stevanovic Natasa Kovacevic-Grujicic Marija Mojsin Milena Milivojevic Danijela Drakulic laboratory for Human molecular genetics Institute of Molecular Genetics and Genetic EngineeringUniversity of BelgradeBelgrade 11042Serbia Chair Biochemistry and molecular Biology Faculty of BiologyUniversity of BelgradeBelgrade 11158Serbia Department of Chemical and Biological Sciences Serbian Academy of Sciences and ArtsBelgrade 11000Serbia

Glioblastoma(GBM)is the most common,most aggressive and deadliest brain tumor.Recently,remarkable progress has been made towards understanding the cellular and molecular biology of gliomas.GBM tumor initiation,progression and relapse as well as resistance to treatments are associated with glioma stem cells(GSCs).GSCs exhibit a high proliferation rate and self-renewal capacity and the ability to differentiate into diverse cell types,generating a range of distinct cell types within the tumor,leading to cellular heterogeneity.GBM tumors may contain different subsets of GSCs,and some of them may adopt a quiescent state that protects them against chemotherapy and radiotherapy.GSCs enriched in recurrent gliomas acquire more aggressive and therapy-resistant properties,making them more malignant,able to rapidly spread.The impact of SOX transcription factors(TFs)on brain tumors has been extensively studied in the last decade.Almost all SOX genes are expressed in GBM,and their expression levels are associated with patient prognosis and survival.Numerous SOX TFs are involved in the maintenance of the stemness of GSCs or play a role in the initiation of GSC differentiation.The fine-tuning of SOX gene expression levels controls the balance between cell stemness and differentiation.Therefore,innovative therapies targeting SOX TFs are emerging as promising tools for combatting GBM.Combatting GBM has been a demanding and challenging goal for decades.The current therapeutic strategies have not yet provided a cure for GBM and have only resulted in a slight improvement in patient survival.Novel approaches will require the fine adjustment of multimodal therapeutic strategies that simultaneously target numerous hallmarks of cancer cells to win the battle against GBM.

关键词： Glioblastoma SOX transcription factors Glioma stem cells Stemness Differentiation

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Marsdenia tenacissima injection induces the apoptosis of prostate cancer by regulating the AKT/GSK3β/STAT3 signaling axis

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Chinese Journal of Natural Medicines 2023年第2期21卷 113-126页

作者： LI Xiaolan HE Songhua LIANG Wei ZHANG Weiquan CHEN Xin LI Qiaofeng YANG Xin LIU Yanying ZHU Dan LI Li LIU Buming SU Zhiheng CHEN Jie GUO Hongwei Guangxi Key laboratory of Bioactive Molecules Research and Evaluation&College of Pharmacy Guangxi Medical UniversityNanning 530021China Key laboratory of Longevity and aging-related Diseases of Chinese Ministry of Education&Center for Translational Medicine Guangxi Medical UniversityNanning 530021China Guangxi Institute for Food and Drug Control Drug Administration of Zhuang Autonomous RegionNanning 530021China Guangxi Key laboratory of Traditional Chinese Medicine Quality Standards Guangxi Institute of Chinese Medicine&Pharmaceutical ScienceNanning 530022China The Affiliated tumor Hospital Guangxi Medical UniversityNanning 530021China

Marsdenia tenacissima injection,a standard Marsdenia tenacissima extract(MTE),has been approved as an adjuvant therapeutic agent for various cancers.Our previous study showed that MTE inhibited the proliferation and metastasis of prostate cancer(PCa)cells.However,the underlying mechanisms and active ingredients of MTE against PCa were not completely understood.This study revealed that MTE induced significant decreases in cell viability and clonal growth in PCa cells.In addition,MTE induced the apoptosis of DU145 cells by reducing the mitochondrial membrane potential and increasing the expression of Cleaved Caspase 3/7,Cyt c,and Bax.In vivo,DU145 xenografted NOD-SCID mice treated with MTE showed significantly decreased tumor size.TUNEL staining and Western blot confirmed the pro-apoptotic effects of MTE.Network pharmacology analysis collected 196 ingredients of MTE linked to 655 potential targets,and 709 PCa-associated targets were retrieved,from which 149 overlapped targets were screened out.Pathway enrichment analysis showed that the HIF-1,PI3K-AKT,and ErbB signaling pathways were closely related to tumor apoptosis.Western blot results confirmed that MTE increased the expression of p-AKT^(Ser473) and p-GSK3β^(Ser9),and decreased the expression of p-STAT3^(Tyr705) in vitro and in vivo.A total of 13 compounds in MTE were identified by HPLC-CAD-QTOF-MS/MS and UPLCQTOF-MS/MS.molecular docking analysis indicated that six compounds may interact with AKT,GSK3β,and STAT3.In conclusion,MTE induces the endogenous mitochondrial apoptosis of PCa by regulating the AKT/GSK3β/STAT3 signaling axis,resulting in inhibition of PCa growth in vitro and in vivo.

关键词： Marsdenia tenacissima injection Prostate cancer Apoptosis AKT/GSK3β/STAT3

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molecular regulation of telomerase activity in aging

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Protein & Cell 2011年第9期2卷 726-738页

作者： Craig Nicholls He Li Jian-Qiu Wang Jun-Ping Liu molecular Signalling laboratory Murdoch Childrens Research InstituteFlemington RoadParkvilleVictoria 3052Australia Institute of aging Research Hangzhou Normal University School of MedicineHangzhou 310036China Department of Immunology Monash UniversityMelbourneVictoria 3004Australia Department of genetics University of MelbourneVictoria 3052Australia

The process of aging is mitigated by the maintenance and repair of chromosome ends(telomeres),resulting in extended lifespan.This review examines the molecular mechanisms underlying the actions and regulation of the enzyme telomerase reverse transcriptase(TERT),which functions as the primary mechanism of telomere maintenance and regulates cellular life expectancy.Underpinning increased cell proliferation,telomerase is also a key factor in facilitating cancer cell immortalization.The review focuses on aspects of hormonal regulations of telomerase,and the intracellular pathways that converge to regulate telomerase activity with an emphasis on molecular interactions at protein and gene levels.In addition,the basic structure and function of two key telomerase enzyme components—the catalytic subunit TERTand the template RNA(TERC)are discussed briefly.

关键词： telomerase aging telomerase reverse transcriptase(TERT)

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Neuroendocrine and squamous colonic composite carcinoma:Case report with molecular analysis

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World Journal of Gastroenterology 2011年第42期17卷 4729-4733页

作者： Sabrina C Wentz Cindy Vnencak-Jones William V Chopp Department of Pathology Vanderbilt University Medical Center molecular genetics laboratory Vanderbilt University Medical Center Department of Pathology Veterans Affairs Medical Center

Composite colorectal carcinomas are rare. There are amodest number of cases in the medical literature,with even fewer cases describing composite carcinoma with neuroendocrine and squamous components. There areto our knowledge no reports of composite carcinomamolecular alterations. We present a case of composite carcinoma of the splenic flexure in a 33 year-old Cau-casian male to investigate the presence and prognos-tic significance of molecular alterations in rare coloniccarcinoma subtypes. Formalin-fixed paraffin-embedded(FFPE) tissue was hematoxylin and eosin- and mucicar-mine-stained according to protocol,and immuno-stained with cytokeratin(CK) 7,CK20,CDX2,AE1/AE3,chromo-granin-A and synaptophysin. DNA was extracted from FFPE tissues and molecular analyses were performed according to lab-developed methods,followed by capil-lary electrophoresis. Hematoxylin and eosin staining showed admixed neuroendocrine and keratinized squamous cells. Positive nuclear CDX2 expression confirme dintestinal derivation. CK7 and CK20 were negative.Neuroendocrine cells stained positively for synaptophysin and AE1/AE3 and negatively for chromogranin and mucicarmine. Hepatic metastases showed a similar immunohistochemical profile. molecular analysis revealeda G13D KRAS mutation. BRAF mutational testing wasnegative and microsatellite instability was not detected.The patient had rapid disease progression on chemotherapy and died 60 d after presentation. Although theG13D KRAS mutation normally predicts an intermed iateoutcome,the aggressive tumor behavior suggests other modifying factors in rare types of colonic carcinomas.

关键词：神经内分泌细胞复合材料分子分析生物学分析大肠癌结肠癌病例报告石蜡包埋组织

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AQR is a novel type 2 diabetes-associated gene that regulates signaling pathways critical for glucose metabolism

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Journal of genetics and Genomics 2018年第2期45卷 111-120页

作者： Chun Song Han Yan Hanming Wang Yan Zhang Huiqing Cao Yiqi Wan Lingbao Kong Shenghan Chen Hong Xu Bingxing Pan Jin Zhang Guohuang Fan Hongbo Xin Zicai Liang Weiping Jia Xiao-Li Tian laboratory of Human Population genetics Institute of Molecular Medicine Peking University Beijing 100871 China State Key laboratory of Membrane Biology Institute of Molecular Medicine Peking University Beijing 100871 China Beijing Key laboratory of Cardiometabolic molecular Medicine Peking University Beijing 100871 China laboratory of Nucleic Acid Technology Institute of Molecular Medicine Peking University Beijing 100871 China Human Population genetics Human Aging Research Institute and School of Life Sciences Nanchang University Nanchang 330006 China Institute of Life Science and School of Life Science Nanchang University Nanchang 330031 China School of Basic Medical Sciences Nanchang University Nanchang 330006 China Institute of Translational Medicine Nanchang University Nanchang 330031 China Shanghai Key laboratory of Diabetes Mellitus and Center for Translational Medicine Shanghai Jiao Tong University Affiliated Sixth People's HospitalShanghai 200233 China

Type 2 diabetes mellitus（T2 DM） is a common metabolic disease influenced by both genetic and environmental factors. In this study, we performed an in-house genotyping and meta-analysis study using three independent GWAS datasets of T2 DM and found that rs3743121, located 1 kb downstream of AQR,was a novel susceptibility SNP associated with T2 DM. The risk allele C of rs3743121 was correlated with the increased expression of AQR in white blood cells, similar to that observed in T2 DM models. The knockdown of AQR in HepG2 facilitated the glucose uptake, decreased the expression level of PCK2,increased the phosphorylation of GSK-3β, and restored the insulin sensitivity. Furthermore, the suppression of AQR inhibited the mTOR pathway and the protein ubiquitination process. Our study suggests that AQR is a novel type 2 diabetes-associated gene that regulates signaling pathways critical for glucose metabolism.

关键词： Type 2 diabetes AQR Glucose metabolism Ubiquitination

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Rb Protein is Essential to the Senescence-Associated Heterochromatic Foci Formation Induced by HMGA2 in Primary WI38 Cells

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Journal of genetics and Genomics 2013年第8期40卷 391-398页

作者： Xi Shi Baoqing Tian Lingxia Liu Yanyan Gao Chi Ma Namusamba Mwichie Wenlong Ma Liping Han Baiqu Huang Jun Lu Yu Zhang The Key laboratory of molecular Epigenetics of the Ministry of Education Northeast Normal University The Institute of genetics and Cytology Northeast Normal University School of Life Sciences Changchun Normal University

Cellular senescence is an irreversible form of cell cycle arrest that provides a barrier to neoplastic transformation. The integrity of the Rb （Retinoblastoma） pathway is necessary for the formation of the senescence-associated heterochromatin foci （SAHF） that offers a molecular basis for the stability of the senescent state. Surprisingly, although high mobility group A2 protein （HMGA2） can promote tumorigenesis and inhibit Rb function in tumor cells, high-level expression of HMGA2 is sufficient to induce SAHF formation in primary cells. It therefore becomes significant to determine whether Rb protein is necessary in HMGA2-induced SAHF formation. In this study, we established the cellular senescence and SAHF assembly W138 cell model by ectopic expression of HMGA2, in which typical senescent markers were seen, including notable upregulation of p53, p21 and p16, and elevated SA-[3-galactosidase staining together with downregulation of E2F target genes. We then showed that the Rb pathway inhibitor E7 protein was able to partly abolish the ability of SAHF formation alter HMGA2 expression in W138 cells, indicating that Rb is a crucial factor for HMGA2-induced SAHF formation. However. Rb depletion did not completely rescue the cell growth arrest induced by HMGA2, suggesting that Rb is not an exclusive pathway for HMGA2-induced senescence in W138 cells.

关键词： HMGA2： SAHF Cellular senescence Rb

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Phytic acid-modified CeO_(2) as Ca^(2+) inhibitor for a security reversal of tumor drug resistance

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Nano Research 2022年第5期15卷 4334-4343页

作者： Zhimin Tian Junlong Zhao Shoujie Zhao Huicheng Li Zhixiong Guo Zechen Liang Jiayuan Li Yongquan Qu Dongfeng Chen Lei Liu Department Key laboratory of Special Functional and Smart Polymer Materials of Ministry of Industry and Information Technology School of Chemistry and Chemical EngineeringNorthwestern Polytechnical UniversityXi’an 710072China State Key laboratory of Cancer Biology Department of Medical Genetics and Developmental BiologyFourth Military Medical UniversityXi’an 710032China Department of General Surgery Tangdu HospitalFourth Military Medical UniversityXi’an 710038China The State Key laboratory of Cancer Biology Department of Biochemistry and Molecular BiologySchool of Basic MedicineFourth Military Medical UniversityXi’an 710032China Department of Gastroenterology Daping HospitalArmy Medical UniversityChongqing 400042China

Ca^(2+)plays critical roles in the development of diseases,whereas existing various Ca regulation methods have been greatly restricted in their clinical applications due to their high toxicity and inefficiency.To solve this issue,with the help of Ca overexpressed tumor drug resistance model,the phytic acid(PA)-modified CeO_(2) nano-inhibitors have been rationally designed as an unprecedentedly safe and efficient Ca2+inhibitor to successfully reverse tumor drug resistance through Ca^(2+)negative regulation strategy.Using doxorubicin(Dox)as a model chemotherapeutic drug,the Ca^(2+)nano-inhibitors efficiently deprived intracellular excessive free Ca2+,suppressed P-glycoprotein(P-gp)expression and significantly enhanced intracellular drug accumulation in Dox-resistant tumor cells.This Ca^(2+)negative regulation strategy improved the intratumoral Dox concentration by a factor of 12.4 and nearly eradicated tumors without obvious adverse effects.Besides,nanocerias as pH-regulated nanozyme greatly alleviated the adverse effects of chemotherapeutic drug on normal cells/organs and substantially improved survivals of mice.We anticipate that this safe and effective Ca^(2+)negative regulation strategy has potentials to conquer the pitfalls of traditional Ca inhibitors,improve therapeutic efficacy of common chemotherapeutic drugs and serves as a facile and effective treatment platform of other Ca^(2+) associated diseases.

关键词： Ca^(2+)nano-inhibitor nanoceria tumor drug resistance phytic acid nanozyme

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Model systems to study the life cycle of human papillomaviruses and HPV-associated cancers

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Virologica Sinica 2015年第2期30卷 92-100页

作者： Louise T.Chow Department of Biochemistry and molecular genetics University of Alabama at Birmingham Birmingham 35294-0005 USA

The prevalent human papillomaviruses(HPVs) infect either cutaneous or mucosal epithelium. Active Infections lead to epithelial hyperprolifeation and are usually cleared in healthy individuals within a year. Persistent infections in the anogenital tracts by certain high-risk genotypes such as HPV-16, HPV-18 and closely related types, can progress to high grade dysplasias and carcinomas in women and men, including cervical, vulva, penile and anal cancers. A significant fraction of the head and neck cancers are also caused by HPV-16. The viral oncogenes responsible for neoplastic conversion are E6 and E7 that disrupt the pathways controlled by the two major tumor suppressor genes, p53 and members of p RB family. Because HPV cannot be propagated in conventional submerged monolayer cell cultures, organotypic epithelial raft cultures that generate a stratified and differentiated epithelium have been used to study the viral life cycle. This article describes several systems to examine aspects of the viral productive phase, along with the advantages and limitations. Animal model systems of HPV carcinogenesis are also briefly described.

关键词： human papillomaviruses(HPVs) productive program HPV-associated cancers model systems

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Antioxidant Potential of Four Species of Natural Product and Therapeutic Strategies for Cancer through Suppression of Viability in the Human Multiple Myeloma Cell Line U266

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Biomedical and Environmental Sciences 2019年第1期32卷 22-33页

作者： Guesmi Fatma Saidi Issam Soussi Rawya Hfaiedh Najla Landoulsi Ahmed laboratory of Biochemistry and molecular Biology Faculty of Sciences of Bizerte University of Carthage Research Unit of Macromolecular Biochemistry and genetics Faculty of Sciences of Gfasa laboratory of Animal Eco Physiology Faculty of Sciences of Gafsa laboratory of Integrated Physiology Faculty of Science of Bizerte University of Carthage

Objective This research aimed to evaluate the protective effects of bioactive compounds such as phenolic acids, flavonoids, and tannins present in four species extracted with methanol. Methods The total phenolic content of the methanolic extracts was measured spectrophotometrically. The effect of the extracts on cell viability in U266 cells was measured. The effects of extracts on free radical scavenging were assessed by the DPPH test and FRAP assay. Antibacterial effects of the natural products in this report were investigated by using the disc diffusion method. Results Our results clearly demonstrated that the methanolic extracts were characterized by a high amount of phenolic compounds. It has been speculated that ME-TA and ME-TAl exhibit a significant(P tumor suppressors.

关键词： Methanolic fractions Phenolic content DPPH FRAP U266 Antibacterial effect

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Enzyme-triggered deep tumor penetration of a dual-drug nanomedicine enables an enhanced cancer combination therapy

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Bioactive Materials 2023年第8期26卷 102-115页

作者： Lei Gu Zhenyu Duan Xue Li Xin Li Yinggang Li Xiaoling Li Gang Xu Peng Gao Hu Zhang Zhongwei Gu Jie Chen Qiyong Gong Kui Luo Huaxi MR Research Center(HMRRC) Department of RadiologyFrontiers Science Center for Disease-Related Molecular NetworkState Key Laboratory of BiotherapyWest China HospitalSichuan UniversityChengdu610041China Liver Transplant Center Organ Transplant CenterBreast CenterLaboratory of Stem Cell BiologyLaboratory of Clinical Proteomics and MetabolomicsInstitutes for Systems GeneticsNational Clinical Research Center for GeriatricsWest China HospitalSichuan UniversityChengduSichuanChina Amgen Bioprocessing Centre Keck Graduate InstituteClaremontCA91711USA Functional and molecular Imaging Key laboratory of Sichuan Province Key Laboratory of Transplant Engineering and ImmunologyNHCResearch Unit of PsychoradiologyChinese Academy of Medical SciencesChengdu610041China Department of Radiology West China Xiamen Hospital of Sichuan UniversityXiamen361000FujianChina

Cancer cells could be eradicated by promoting generation of excessive intracellular reactive oxygen species(ROS)via emerging nanomedicines.However,tumor heterogeneity and poor penetration of nanomedicines often lead to diverse levels of ROS production in the tumor site,and ROS at a low level promote tumor cell growth,thus diminishing the therapeutic effect of these nanomedicines.Herein,we construct an amphiphilic and block polymer-dendron conjugate-derived nanomedicine(Lap@pOEGMA-b-p(GFLG-Dendron-Ppa),GFLG-DP/Lap NPs)that incorporates a photosensitizer,Pyropheophorbide a(Ppa),for ROS therapy and Lapatinib(Lap)for molecular targeted therapy.Lap,an epidermal growth factor receptor(EGFR)inhibitor that plays a role in inhibiting cell growth and proliferation,is hypothesized to synergize with ROS therapy for effectively killing cancer cells.Our results suggest that the enzyme-sensitive polymeric conjugate,pOEGMA-b-p(GFLG-Dendron-Ppa)(GFLG-DP),releases in response to cathepsin B(CTSB)after entering the tumor tissue.Dendritic-Ppa has a strong adsorption capacity to tumor cell membranes,which promotes efficient penetration and long-term retention.Lap can also be efficiently delivered to internal tumor cells to play its role due to the increased vesicle activity.Laser irradiation of Ppa-containing tumor cells results in production of intracellular ROS that is sufficient for inducing cell apoptosis.Meanwhile,Lap efficiently inhibits proliferation of remaining viable cells even in deep tumor regions,thus generating a significant synergistic anti-tumor therapeutic effect.This novel strategy can be extended to the development of efficient membrane lipid-based therapies to effectively combat tumors.

关键词： Proliferation inhibition Apoptosis Amphiphilic and block polymer-dendron conjugate Enhanced penetration Membrane flow Combination therapy

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