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Understanding cancer stem cell heterogeneity and plasticity

细胞研究（英文版） 2012年第3期22卷 457-472页

作者： Dean G Tang Department of Molecular Carcinogenesis the University of Texas M D.Anderson Cancer Center Science Park 1808 Park Rd.1C Smithville TX 78957 USA Program in Environmental & Molecular Carcinogenesis Graduate School of Biomedical Sciences(GSBS) Houston TX 77030 USA Centers for Cancer Epigenetics Stem Cell and Developmental Biology RNA Interference and Non-coding RNAs and Molecular Carcinogenesis the University of Texas M.D.Anderson Cancer Center Houston TX 77030USA Cancer Stem Cell Institute Research Center for Translational Medicine East Hospital Tongji University Shanghai 200120China

Heterogeneity is an omnipresent feature of mammalian cells in vitro and in vivo. It has been recently realized that even mouse and human embryonic stem cells under the best culture conditions are heterogeneous containing pluripotent as well as partially committed cells. Somatic stem cells in adult organs are also heterogeneous, containing many subpopulations of self-renewing cells with distinct regenerative capacity. The differentiated progeny of adult stem cells also retain significant developmental plasticity that can be induced by a wide variety of experimental approaches. Like normal stem cells, recent data suggest that cancer stem cells (CSCs) similarly display significant phenotypic and functional heterogeneity, and that the CSC progeny can manifest diverse plasticity. Here, I discuss CSC heterogeneity and plasticity in the context of tumor development and progression, and by comparing with normal stem cell development. Appreciation of cancer cell plasticity entails a revision to the earlier concept that only the tumorigenic subset in the tumor needs to be targeted. By understanding the interrelationship between CSCs and their differentiated progeny, we can hope to develop better therapeutic regimens that can prevent the emergence of tumor cell variants that are able to found a new tumor and distant metastases.

关键词： cancer stem cells heterogeneity plasticity reprogramming

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The DrugPattern tool for drug set enrichment analysis and its prediction for beneficial effects of oxLDL on type 2 diabetes

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Journal of Genetics and Genomics 2018年第7期45卷 389-397页

作者： Chuanbo Huang Weili Yang Junpei wang Yuan Zhou Bin Geng Georgios Kararigas Jichun Yang Qinghua Cui Department of Biomedical Informatics Department of Physiology and Pathophysiology MOE Key Lab of Cardiovascular Sciences School of Basic Medical Sciences Center for Non-Coding RNA Medicine Peking UniversityBeijing 100191China School of Mathematics Sciences Huaqiao University Quanzhou 362021 China Hypertension Center Fuwai Hospital Chinese Academy of Medical Sciences and Peking Union Medical CollegeState Key Laboratory of Cardiovascular Disease National Center for Cardiovascular Diseases Beijing 100037 China Charit-Universitatsmedizin Berlin. Corporate Member of Freie Universitat Berlin Humboldt-Universitat zu Berlin Berlin Institute of Health Institute of Gender in Medicine and Center for Cardiovascular Research. DZHK (German Centre for Cardiovascular Research) 10115 Berlin Germany Center of Bioinformatics Key Laboratory for Neuro-lnformation of Ministry of Education School of Life Science and Technology University of Electronic Science and Technology of China Chengdu 610054 China

Enrichment analysis methods, e.g., gene set enrichment analysis, represent one class of important bio- informatical resources for mining patterns in biomedical datasets. However, tools for inferring patterns and rules of a list of drugs are limited. In this study, we developed a web-based tool, DrugPattern, for drug set enrichment analysis. We first collected and curated 7019 drug sets, including indications, adverse reactions, targets, pathways, etc. from public databases. For a list of interested drugs, DrugPat- tern then evaluates the significance of the enrichment of these drugs in each of the 7019 drug sets. To validate DrugPattern, we employed it for the prediction of the effects of oxidized low-density lipoprotein （oxLDL）, a factor expected to be deleterious. We predicted that oxLDL has beneficial effects on some diseases, most of which were supported by evidence in the literature. Because DrugPattern predicted the potential beneficial effects of oxLDL in type 2 diabetes （T2D）, animal experiments were then performed to further verify this prediction. As a result, the experimental evidences validated the DrugPattern prediction that oxLDL indeed has beneficial effects on T2D in the case of energy restriction. These data confirmed the prediction accuracy of our approach and revealed unexpected protective roles for oxLDL in various diseases. This study provides a tool to infer patterns and rules in biomedical datasets based on drug set enrichment analysis.

关键词： Enrichment analysis Drug Data mining oxLDL Type 2 diabetes

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OUGENE： a disease associated over-expressed and under-expressed gene database

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Science Bulletin 2016年第10期61卷 752-754页

作者： Xiaoyong Pan Hong-Bin Shen Section for Animal Genetics Bioinformatics and Breeding Center for Non-Coding RNA in Technology and Health University of Copenhagen 1870 Frederiksberg Denmark Department of Disease Systems Biology Novo NordiskFoundation Center for Protein Research University ofCopenhagen 1870 Frederiksberg Denmark Institute of Image Processing and Pattern Recognition Shanghai Jiao Tong University and Key Laboratory of System Control and Information Processing Ministry of Education of China Shanghai 200240 China

Gene over-expression or under-expression is closely associated with human diseases, which contributes to phenotypic variations and diversity. To our best knowledge, there is no single open specific resource available to provide the association information between gene over- or under-expression and various diseases. In this study, we presented a comprehensive disease-associated over- and under-expressed gene database （OUGene） based on our proposed text mining pipeline and several open curated databases. It contains total 41,269 unique associa- tions between 7,238 over- or under-expressed genes and 1,480 diseases, which are supported by 81,974 evidence sentences from 56,442 articles. The OUGene is compre- hensive and covers most important therapeutic areas. Meanwhile a new scoring system is designed to rank the associations based on benchmarking against hand-curated data. OUGene provides an easy-of-use web interface for researchers to analyze these data and visualize the associ- ated networks, which can give insights to the complex relationships between over- and under-expressed genes and diseases at a system level. It is available at ***. ***/bioinf/OUGene/.

关键词： Text mining Gene over- and under-expression Disease Database

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Deep rna-Seq analysis reveals unexpected features of human prostate basal epithelial cells

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Genomics Data 2016年 7卷 318-320页

作者： Dingxiao Zhang Daechan Park Yue Lu Jianjun Shen Vishwanath R. Iyer Dean G. Tang Department of Epigenetics and Molecular Carcinogenesis University of Texas MD Anderson Cancer Center Smithville TX 78957 United States Institute for Cellular and Molecular Biology Center for Systems and Synthetic Biology and Section of Molecular Genetics and Microbiology University of Texas at Austin Austin TX 78712-0159 United States Centers for Cancer Epigenetics Stem Cell and Developmental Biology RNA Interference and Non-Coding RNAs and Molecular Carcinogenesis University of Texas MD Anderson Cancer Center Houston TX United States

Prostate cancer is the second leading cause of cancer-related deaths among American men [ 1 ]. The prostate gland mainly contains basal and luminal cells, which are constructed as a pseudostratified epithelium. Annotation of prostate epithelial transcriptomes provides a foundation for discoveries that can impact disease understanding and treatment. Here, for the first time, we describe a whole-genome transcriptome analysis of human benign prostatic basal and luminal populations by using deep rna sequencing (GSE67070) [2]. Combined with comprehensive molecular and biological characterizations, we show that the differential gene expression profiles account for their distinct functional phenotypes. Strikingly, in contrast to luminal cells, basal cells preferentially express gene categories associated with stem cells, neural and neuronal development, and rna processing. Of clinical relevance, the treatment failed castration-resistant and anaplastic prostate cancers molecularly resemble a basal-like phenotype. We also identified genes associated with patient clinical outcome. Therefore, we provide a gene expression resource for understanding human prostate epithelial lineages, and link the cell-type specific gene signatures to subtypes of prostate cancer development.

关键词： Prostate epithelial cells Basal cells Luminal cells rna-seq

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Simultaneous Targeting of Tumor Cells and Tumor-Associated Macrophages To Reprogram Glioblastoma Using Trypsinized Extracellular Vesicles Carrying Tumor Suppressive Microrna

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Nano Letters 2025年第20期25卷 2025 May 13页

作者： Nguyen, Grace H. Noh, MinHye Kang, Jin Muk Miller, Alexandra A. Huang, Minxin Kim, Jiyeon Lee, Jeong-Yeon Chung, Sangwoon Wang, Hongyu Calin, George A. Ju, Cynthia Eltzschig, Holger K. Banasavadi-Siddegowda, Yeshavanth Zhao, Zhongming Yoo, Ji Young Lee, Tae Jin Department of Neurosurgery McGovern Medical School University of Texas Health Science Center at Houston 6431 Fannin Street Houston 77030 TX United States Graduate School of Biomedical Sciences The University of Texas MD Anderson Cancer Center-UT Health at Houston 6767 Bertner Avenue Houston 77030 TX United States Department of Pathology College of Medicine Hanyang University 222 Wangsimni-ro Seongdong-gu Seoul 04763 South Korea Pulmonary Allergy Critical Care and Sleep Medicine The Ohio State University Wexner Medical Center Davis Heart Lung Research Institute 473 W 12th Avenue Columbus 43210 OH United States Department of Diagnostic and Interventional Imaging McGovern Medical School University of Texas Health Science Center at Houston 6901 Bertner Avenue Houston 77030 TX United States Department of Translational Molecular Pathology Division of Pathology-Lab Medicine Center for RNA Interference Non-Coding RNAs The University of Texas MD Anderson Cancer Center 1881 East Road Houston 77054 TX United States Department of Anesthesiology Critical Care and Pain Medicine McGovern Medical School University of Texas Health Science Center at Houston 6431 Fannin Street Houston 77030 TX United States Surgical Neurology Branch National Institute of Neurological Disorders and Stroke National Institutes of Health 9000 Rockville Pike Bethesda 20892 MD United States Center for Precision Health McWilliams School of Biomedical Informatics University of Texas Health Science Center at Houston 7000 Fannin Street Houston 77030 TX United States

Glioblastoma (GBM) remains difficult to treat due to poor drug delivery across the blood-brain barrier and an immunosuppressive tumor microenvironment (TME). Tumor-suppressive micrornas (mirnas) offer a promising strategy to reprogram both tumor cells and the TME, but inefficient delivery systems limit their clinical application. We previously reported that tumor-suppressive miR-138 regresses tumor growth in preclinical GBM models. Here, we demonstrate that trypsin digestion of extracellular vesicles (EVs) enhances labeling efficiency with folate (FA), enhancing selective targeting of folate receptor (FR)-positive GBM cells and enabling simultaneous targeting of tumor-associated macrophages (TAMs). FA-labeled trypsinized EVs (tEVs) loaded with miR-138 inhibit tumor growth, depolarize TAMs, and enhance antitumor immunity. This study represents the first preclinical attempt to modulate tumor cells and innate immunity via mirna-loaded tEVs, offering a novel and more effective therapeutic approach to GBM treatment. © 2025 American Chemical Society.

关键词： Extracellular vesicle (EV) Glioblastoma (GBM) microrna-138 (miR-138) Trypsin Tumor microenvironment (TME) Tumor-associated macrophages (TAMs)

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Structural and Functional Research of ALS Associated Protein FUS(fused in sarcoma)

Structural and Functional Research of ALS Associated Protein...

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第一届国际暨第十三次中国生物物理学术大会

作者： Chunyan Niu Xuehui Liu Jintao Ren Minze Jia Feng Gao Wei Feng Haining Zhu Weimin Gong Laboratory of Non-coding RNA Institute of BiophysicsChinese Academy of Sciences National Laboratory of Biomacromolecules Institute of BiophysicsChinese Academy of Sciences Department of Molecular and Cellular Biochemistry & Center for Structural Biology College of MedicineUniversity of Kentucky741 South LimestoneLexingtonKY 40536USA

Fused in sarcoma/translocated in liposarcoma(FUS/TLS)is a DNA/rna binding protein that is involved in many processes of rna metabolism including gene transcription regulation,rna splicing and transport,translation,process of micro rnas,and maintenance of genomic *** have been recently reported to cause a familial form of amyotrophic lateral sclerosis(ALS).This study solved the crystal structure of FUS-NLS/Transportin 1 *** binding

关键词： ALS rna fused in sarcoma Structural and Functional Research of ALS Associated Protein FUS

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Diagnostic and Therapeutic Micrornas in Primary Myelofibrosis

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Proceedings of the Singapore National Academy of Science 2020年第2期14卷 91-109页

作者： Roxana Manaila Vlad Moisoiu Erik Knutsen Mihnea P. Dragomir George A. Calin Clinical Institute of Urology and Renal Transplantation Cluj-Napoca Romania Contributed equally to this manuscript. Faculty of Physics Babeş-Bolyai University Cluj-Napoca Romania Department of Medical Biology Faculty of Health Sciences UiT — The Arctic University of Norway Tromsø Norway Department of Surgery Fundeni Clinical Hospital Carol Davila University of Medicine and Pharmacy Bucharest Romania Department of Experimental Therapeutics The University of Texas MD Anderson Cancer Center Houston TX USA The Center for RNA Interference and Non-Coding RNAs The University of Texas MD Anderson Cancer Center Houston TX USA

Primary myelofibrosis (PMF) is a pluripotent hematopoietic stem cell-derived malignancy, included in the heterogeneous group of myeloproliferative neoplasms (MPNs). PMF diagnosis is based on a composite assessment of clinical and laboratory data. The three major diagnostic criteria are: screening for driver mutations, exclusion of other conditions that can cause myelofibrosis, and bone marrow biopsy displaying megakaryocyte changes and fibrosis. PMF treatment options are only partially disease-modifying and consist mainly of symptom control. Recently, a new targeted therapy was introduced for PMF patients, JAK-STAT inhibitors (i.e. ruxolitinib). However, specific subgroups of patients do not benefit from the JAK-STAT inhibitors: (1) those who are carrying JAK2 mutations, but ruxolitinib does not reduce the spleen size; (2) triple negative patients (no JAK2 , CALR , or MPL mutations); and (3) those who discontinue JAK-STAT therapy because of side effects. These subgroups are in need of new therapeutic approaches. Mature micrornas (mirnas) range from 16 to 28 nucleotides (nt) in length and regulate specific messenger rnas at the post-transcriptional level. Numerous in vitro and in vivo studies have reported specific mirnas, as well as complex mirna networks, to be dysregulated in PMF. Several of these mirnas were shown to be implicated in essential events of PMF pathophysiology: increase of bone marrow fibrosis, progression to acute myeloid leukemia, resistance to JAK-STAT inhibitors, and activation of differentiation of hematopoietic stem/progenitor cells into megakaryocytes. Hence, we propose mirnas as a potential minimally invasive diagnostic tool for PMF and as therapeutic targets that could address the unmet medical needs of these patients.

关键词： Primary myelofibrosis myeloproliferative neoplasms microrna network theory JAK-STAT inhibitors ruxolitinib miR-379/656 cluster microrna therapy

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TISSUES 2.0: an integrative web resource on mammalian tissue expression (vol 2018, 2018)

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DATABASE-THE JOUrnaL OF BIOLOGICAL DATABASES AND CURATION 2018年第2018期2018卷 1-N.PAG页

作者： Palasca, Oana Santos, Alberto Stolte, Christian Gorodkin, Jan Jensen, Lars Juhl Novo Nordisk Foundation Center for Protein Research Faculty of Health and Medical Sciences University of Copenhagen Copenhagen DenmarkCenter for non-coding RNA in Technology and Health Faculty of Health and Medical Sciences University of Copenhagen Copenhagen DenmarkDepartment of Veterinary and Animal Sciences Faculty of Health and Medical Sciences University of Copenhagen Copenhagen Denmark Novo Nordisk Foundation Center for Protein Research Faculty of Health and Medical Sciences University of Copenhagen Copenhagen Denmark New York Genome Center New York NY USA Center for non-coding RNA in Technology and Health Faculty of Health and Medical Sciences University of Copenhagen Copenhagen DenmarkDepartment of Veterinary and Animal Sciences Faculty of Health and Medical Sciences University of Copenhagen Copenhagen Denmark Correspondence may also be addressed to Jan Gorodkin. Email: gorodkin@rth.dk Novo Nordisk Foundation Center for Protein Research Faculty of Health and Medical Sciences University of Copenhagen Copenhagen DenmarkCenter for non-coding RNA in Technology and Health Faculty of Health and Medical Sciences University of Copenhagen Copenhagen Denmark Corresponding author: Tel: +45 35325025 Email: lars.juhl.jensen@cpr.ku.dk

Physiological and molecular similarities between organisms make it possible to translate findings from simpler experimental systems—model organisms—into more complex ones, such as human. This translation facilitates the understanding of biological processes under normal or disease conditions. Researchers aiming to identify the similarities and differences between organisms at the molecular level need resources collecting multi-organism tissue expression data. We have developed a database of gene-tissue associations in human, mouse, rat and pig by integrating multiple sources of evidence: transcriptomics covering all four species and proteomics (human only), manually curated and mined from the scientific literature. Through a scoring scheme, these associations are made comparable across all sources of evidence and across organisms. Furthermore, the scoring produces a confidence score assigned to each of the associations. The TISSUES database (version 2.0) is publicly accessible through a user-friendly web interface and as part of the STRING app for Cytoscape. In addition, we analyzed the agreement between datasets, across and within organisms, and identified that the agreement is mainly affected by the quality of the datasets rather than by the technologies used or organisms *** URL: http://***/

关键词： DATABASES TRANSCRIPTOMES PROTEOMICS

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Tissue Transglutaminase Activates Cancer-Associated Fibroblasts and Contributes to Gemcitabine Resistance in Pancreatic Cancer

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NEOPLASIA 2016年第11期18卷 689-698页

作者： Lee, Jiyoon Yakubov, Bakhtiyor Ivan, Cristina Jones, David R. Caperell-Grant, Andrea Fishel, Melissa Cardenas, Horacio Matei, Daniela Indiana Univ Sch Med Dept Otolaryngol Head & Neck Surg Indianapolis IN 46202 USA Indiana Univ Sch Med Dept Med Indianapolis IN 46202 USA Univ Texas MD Anderson Canc Ctr Dept Expt Therapeut Houston TX 77030 USA Univ Texas MD Anderson Canc Ctr Ctr RNA Interference & Non Coding RNAs Houston TX 77030 USA Indiana Univ Sch Med Dept Pediat Indianapolis IN 46202 USA Indiana Univ Melvin & Bren Simon Canc Ctr Indianapolis IN 46204 USA Northwestern Univ Dept Obstet & Gynecol Feinberg Sch Med 303 E Super StLurie 4-107 Chicago IL 60611 USA Robert H Lurie Canc Ctr Chicago IL USA Jesse Brown VA Med Ctr Chicago IL USA

Resistance to chemotherapy is a hallmark of pancreatic ductal adenocarcinoma (PDA) and has been partly attributed to the dense desmoplastic stroma, which forms a protective niche for cancer cells. Tissue transglutaminase (TG2), a Ca2+-dependent enzyme, is secreted by PDA cells and cross-links proteins in the tumor microenvironment (TME) through acyl-transfer between glutamine and lysine residues, promoting PDA growth. The objective of the current study was to determine whether secreted TG2 by PDA cells alters the response of pancreatic tumors to gemcitabine. Orthotopic pancreatic xenografts and co-culture of PDA and stromal cells were employed to determine the mechanisms by which TG2 alters tumor-stroma interactions and response to gemcitabine. Analysis of the pancreatic The Cancer Genome Atlas (TCGA) database demonstrated that increased TG2 expression levels correlate with worse overall survival (hazard ratio = 1.37). Stable TG2 knockdown in PDA cells led to decreased size of pancreatic xenografts and increased sensitivity to gemcitabine in vivo. However, TG2 downregulation did not increase cytotoxicity of gemcitabine in vitro. Additionally, multivessel density and gemcitabine uptake in pancreatic tumor tissue, as measured by mass spectrometry (MS-HPLC), were not significantly different in tumors expressing TG2 versus tumors in which TG2 was knocked down. Fibroblasts, stimulated by TG2 secreted by PDA cells, secrete laminin A1, which protects cancer cells from gemcitabine-induced cytotoxicity. In all, our results demonstrate that TG2 secreted in the pancreatic TME orchestrates the cross talk between cancer cells and stroma, impacting tumor growth and response to chemotherapy. Our study supports TG2 inhibition to increase the antitumor effects of gemcitabine in PDA.

关键词： PANCREATIC cancer treatment TRANSGLUTAMINASES DRUG resistance CHEMOTHERAPY (Cancer) ANTINEOPLASTIC agents FIBROBLASTS

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MiR-506 inhibits multiple targets in the epithelial-to- mesenchymal transition network and is associated with good prognosis in epithelial ovarian cancer

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Journal of Pathology 2015年第1期235卷 25-36页

作者： Sun, Yan Hu, Limei Zheng, Hong Bagnoli, Marina Guo, Yuhong Rupaimoole, Rajesha Rodriguez-Aguayo, Cristian Lopez-Berestein, Gabriel Ji, Ping Chen, Kexin Sood, Anil K. Mezzanzanica, Delia Liu, Jinsong Sun, Baocun Zhang, Wei Department of Pathology Tianjin Medical University Cancer Institute and Hospital Tianjin 300060 China Department of Pathology University of Texas MD Anderson Cancer Center Unit 85 1515 Holcombe Blvd Houston 77030 TX United States Department of Epidemiology and Biostatistics Tianjin Medical University Cancer Institute and Hospital Tianjin 300060 China Department of Experimental Oncology and Molecular Medicine Fondazione IRCCS Istituto Nazionale dei Tumori Milan Italy Department of Gynecologic Oncology and Reproductive Medicine University of Texas MD Anderson Cancer Center Houston 77030 TX United States Center for RNAi and Non-Coding RNA University of Texas MD Anderson Cancer Center Houston 77030 TX United States

Extensive investigations have shown that mirnas are important regulators of epithelial-to-mesenchymal transition (EMT), mainly targeting the transcriptional repressors of E-cadherin (E-cad). Less is known about the post-transcriptional regulation of vimentin or N-cadherin (N-cad) in EMT. Our previous study identified miR-506 as a key EMT inhibitor through directly targeting the E-cad transcriptional repressor SNAI2. In this study, we provide evidence that miR-506 simultaneously suppresses vimentin and N-cad. The knockdown of vimentin using sirna reversed EMT, suppressed cell migration and invasion, and increased E-cad expression on the cell membrane in epithelial ovarian cancer (EOC) cells. In a set of tissue microarrays that included 204 EOCs of all major subtypes (eg serous, endometrioid, clear cell, and mucinous), miR-506 was positively correlated with E-cad and negatively correlated with vimentin and N-cad in all subtypes of EOC. A high level of miR-506 was positively associated with early FIGO stage and longer survival in EOC. Introduction of miR-506, mediated by nanoparticle delivery, in EOC orthotopic mouse models resulted in decreased vimentin, N-cad, and SNAI2 expression and increased E-cad expression;it also suppressed the dissemination of EOC cells. Thus, miR-506 represents a new class of mirna that regulates both E-cad and vimentin/N-cad in the suppression of EMT and metastasis. Copyright © 2014 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

关键词： Epithelial ovarian cancer Epithelial-to-mesenchymal transition miR-506 N-cadherin Nanoparticle Vimentin

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