Sustained proliferation in cancer: Mechanisms and novel therapeutic targets

被引：562

作者：

Feitelson, Mark A. ^{[1
]}

Arzumanyan, Alla ^{[1
]}

Kulathinal, Rob J. ^{[1
]}

Blain, Stacy W. ^{[2
]}

Holcombe, Randall F. ^{[3
]}

Mahajna, Jamal ^{[4
]}

Marino, Maria ^{[5
]}

Martinez-Chantar, Maria L. ^{[6
]}

Nawroth, Roman ^{[7
]}

Sanchez-Garcia, Isidro ^{[8
]}

Sharma, Dipali ^{[9
]}

Saxena, Neeraj K. ^{[10
]}

Singh, Neetu ^{[11
]}

Vlachostergios, Panagiotis J. ^{[12
]}

Guo, Shanchun ^{[13
]}

Honoki, Kanya ^{[14
]}

Fujii, Hiromasa ^{[15
]}

Georgakilas, Alexandros G. ^{[16
]}

Bilsland, Alan ^{[17
]}

Amedei, Amedeo ^{[18
]}

Niccolai, Elena ^{[18
]}

Amin, Amr ^{[19
]}

Ashraf, S. Salman ^{[20
]}

Boosani, Chandra S. ^{[21
]}

Guha, Gunjan ^{[22
]}

Ciriolo, Maria Rosa ^{[23
]}

Aquilano, Katia ^{[23
]}

Chen, Sophie ^{[24
]}

Mohammed, Sulma I. ^{[25
]}

Azmi, Asfar S. ^{[26
]}

Bhakta, Dipita ^{[22
]}

Halicka, Dorota ^{[27
]}

Keith, W. Nicol ^{[17
]}

Nowsheen, Somaira ^{[28
]}

机构：

[1] Temple Univ, Dept Biol, Philadelphia, PA 19122 USA

[2] Suny Downstate Med Ctr, Dept Pediat, Brooklyn, NY 11203 USA

[3] Mt Sinai Sch Med, Tisch Canc Inst, New York, NY USA

[4] MIGAL Galilee Technol Ctr, Canc Drug Discovery Program, Kityat Shmona, Israel

[5] Univ Rome Tre, Dept Sci, I-00146 Rome, Italy

[6] Ctr Invest Biomed Red Enfermedades Hepat & Digest, CIC bioGUNE, Metabol Unit, Technol Pk Bizkaia, Bizkaia, Spain

[7] Tech Univ Munich, Klinikum Rechts Isar, Dept Urol, D-80290 Munich, Germany

[8] Univ Salamanca, CSIC, Inst Biol Mol & Celular Canc, Expt Therapeut & Translat Oncol, E-37008 Salamanca, Spain

[9] Univ Maryland, Sch Med, Dept Med, Baltimore, MD 21201 USA

[10] Johns Hopkins Univ, Sch Med, Dept Oncol, Baltimore, MD 21205 USA

[11] Johns Hopkins Univ, Sidney Kimmel Comprehens Canc Ctr, Baltimore, MD USA

[12] CSIR, Cent Drug Res Inst, Council Sci & Ind Res, Tissue & Cell Culture Unit, Lucknow, Uttar Pradesh, India

[13] NYU, Lutheran Med Ctr, Dept Med, Brooklyn, NY USA

[14] Morehouse Sch Med, Dept Microbiol Biochem & Immunol, Atlanta, GA USA

[15] Nara Med Univ, Dept Orthoped Surg, Kashihara, Nara 634, Japan

[16] Natl Tech Univ Athens, Sch Appl Math & Phys Sci, Dept Phys, Athens 15780, Greece

[17] Univ Glasgow, Inst Canc Sci, Glasgow G12 8QQ, Lanark, Scotland

[18] Univ Florence, Dept Expt & Clin Med, I-50134 Florence, Italy

[19] UAE Univ, Coll Sci, Dept Biol, Al Ain, U Arab Emirates

[20] UAE Univ, Coll Sci, Dept Chem, Al Ain, U Arab Emirates

[21] Creighton Univ, Dept Biomed Sci, Omaha, NE 68178 USA

[22] SASTRA Univ, Sch Chem & Bio Technol, Thanjavur, India

[23] Univ Roma Tor Vergata, Dept Biol, I-00133 Rome, Italy

[24] Ovarian & Prostate Canc Res Trust Lab, Dept Res & Dev, Guildford GU2 7YG, Surrey, England

[25] Purdue Univ, Ctr Canc Res, Dept Comparat Pathobiol, W Lafayette, IN 47907 USA

[26] Wayne State Univ, Sch Med, Karmonas Canc Inst, Dept Pathol, Detroit, MI USA

[27] New York Med Coll, Dept Pathol, Brander Canc Res Inst, Valhalla, NY 10595 USA

[28] Mayo Clin, Med Scientist Training Program, Mayo Med Sch, Mayo Grad Sch, Rochester, MN USA

来源：

SEMINARS IN CANCER BIOLOGY | 2015年 / 35卷

基金：

美国国家科学基金会;

关键词：

Proliferation; Natural products; Therapeutic targets; Cancer stem cells; Cancer hallmarks; NF-KAPPA-B; HUMAN BREAST-CANCER; CELL-CYCLE ARREST; GROWTH-FACTOR-I; ESTROGEN-RECEPTOR-ALPHA; EPITHELIAL-MESENCHYMAL TRANSITION; TELOMERASE-REVERSE-TRANSCRIPTASE; DEPENDENT KINASE INHIBITOR; HEDGEHOG-SIGNALING PATHWAY; ACTIVATED PROTEIN-KINASE;

D O I：

10.1016/j.semcancer.2015.02.006

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Proliferation is an important part of cancer development and progression. This is manifest by altered expression and/or activity of cell cycle related proteins. Constitutive activation of many signal transduction pathways also stimulates cell growth. Early steps in tumor development are associated with a fibrogenic response and the development of a hypoxic environment which favors the survival and proliferation of cancer stem cells. Part of the survival strategy of cancer stem cells may manifested by alterations in cell metabolism. Once tumors appear, growth and metastasis may be supported by overproduction of appropriate hormones (in hormonally dependent cancers), by promoting angiogenesis, by undergoing epithelial to mesenchymal transition, by triggering autophagy, and by taking cues from surrounding stromal cells. A number of natural compounds (e.g., curcumin, resveratrol, indole-3-carbinol, brassinin, sulforaphane, epigallocatechin-3-gallate, genistein, ellagitannins, lycopene and quercetin) have been found to inhibit one or more pathways that contribute to proliferation (e.g., hypoxia inducible factor 1, nuclear factor kappa B, phosphoinositide 3 kinase/Akt, insulin-like growth factor receptor 1, Wnt, cell cycle associated proteins, as well as androgen and estrogen receptor signaling). These data, in combination with bioinformatics analyses, will be very important for identifying signaling pathways and molecular targets that may provide early diagnostic markers and/or critical targets for the development of new drugs or drug combinations that block tumor formation and progression. (C) 2015 Elsevier Ltd.

引用

页码：S25 / S54

页数：30

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