专题论文

PM2.5引起的肿瘤新生血管形成和转移研究进展

  • 孟梅 ,
  • 周泉生
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  • 苏州大学唐仲英血液学研究中心, 苏州 215123
孟梅,硕士研究生,研究方向为肿瘤与血管,电子信箱:mmcatmengmei@163.com

收稿日期: 2014-08-12

  修回日期: 2014-08-15

  网络出版日期: 2014-09-26

基金资助

国家自然科学基金项目(81372376)

Progress in PM2.5-caused Tumor Neovascularization and Metastasis

  • MENG Mei ,
  • ZHOU Quansheng
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  • Cyrus Tang Hematology Center, Soochow University, Suzhou 215123, China

Received date: 2014-08-12

  Revised date: 2014-08-15

  Online published: 2014-09-26

摘要

PM2.5指直径≤2.5 μm 的颗粒物质,它很容易穿过呼吸道屏障,进入血液循环,可诱发肺癌等多种恶性肿瘤,已成为恶性肿瘤新的诱因。近年研究揭示,PM2.5可刺激肿瘤细胞合成和分泌血管内皮生长因子(VEGF),促进血管内皮细胞介导的肿瘤血管新生;并可激活肿瘤细胞,使其通过血管生成拟态直接形成肿瘤血管;还能使肿瘤干细胞向肿瘤内皮细胞转化,促进肿瘤新生血管形成。此外,PM2.5可促进肿瘤细胞及其他多种细胞分泌趋化因子和白细胞介素,招募骨髓和血液中白细胞进入肿瘤组织,诱发局部慢性炎症反应,诱导上皮细胞-间充质细胞转化(EMT)的发生,增加肿瘤细胞干性、迁移和转移能力;还可破坏血管稳态,增加血管通透性,为肿瘤细胞的转移打开方便之门。PM2.5在肿瘤的新生血管形成和转移中起了重要作用,然而,至今对其作用机制知之甚少。因此,进一步深入研究PM2.5诱导的肿瘤新生血管形成及转移机制,能为PM2.5引起的恶性肿瘤防治提供可靠的理论依据和新的应对策略。

本文引用格式

孟梅 , 周泉生 . PM2.5引起的肿瘤新生血管形成和转移研究进展[J]. 科技导报, 2014 , 32(26) : 52 -57 . DOI: 10.3981/j.issn.1000-7857.2014.26.007

Abstract

PM2.5 refers to the particles with 2.5 μm or less in diameter, which can easily go through the barrier of respiratory track and enter the blood circulation. PM2.5 can induce various malignant tumors including lung cancer, and it has become a new cause of cancers. Recent studies have revealed that PM2.5 may stimulate synthesis and secretion of vascular endothelial growth factor (VEGF) and various vascular growth factors, promote vascular endothelial cell-mediated tumor angiogenesis, activate tumor cells and allow cancer cells to directly firm tumor vasculature through vasculogenic mimicry, and induce the trans-differentiation of cancer stem cells into tumor endothelial cells, enhancing tumor neovascularization. In addition, PM2.5 can escalate tumor cells and many other cells to secrete chemokines and cytokines which recruit bone marrow and blood while cells into tumor tissue, and bring about local chronic inflammation. PM2.5 may also induce epithelial-mesenchymal transition (EMT), resulting in an increment of cancer cell stemness, migration, and metastasis. Furthermore, PM2.5 may damage vascular homeostasis system, increase vascular permeation, opening a door for tumor cell metastasis. Taken together, PM2.5 plays important roles in tumor neovascularization and metastasis; whereas, its mechanisms are enigmatic. Thus, more extensive study of the mechanisms of PM2.5-induced tumor neovascularization and metastasis will provide a reliable theory, strategy, and new approach for prevention and treatment of PM2.5-caused malignant tumors in the future.

参考文献

[1] Puett R C, Hart J E, Yanosky J D, et al. Particulate matter air pollution exposure, distance to road, and incident lung cancer in the nurses' health study cohort[J]. Environmental Health Perspectives, 2014, doi: 10.1289/ehp.1307490.
[2] Bakand S, Hayes A, Dechsakulthorn F. Nanoparticles: A review of particle toxicology following inhalation exposure[J]. Inhalation Toxicology, 2012, 24(2): 125-135.
[3] Meng X, Ma Y, Chen R, et al. Size- fractionated particle number concentrations and daily mortality in a Chinese city[J]. Environmental Health Perspectives, 2013, 121(10): 1174-1178.
[4] Hamra G B, Guha N, Cohen A, et al. Outdoor particulate matter exposure and lung cancer: A systematic review and meta-analysis[J]. Environmental Health Perspectives, 2014.
[5] Mahalingaiah S, Hart J E, Laden F, et al. Air pollution and risk of uterine leiomyomata[J]. Epidemiology, 2014, 25(5): 682-688.
[6] Nursan C, Muge A T, Cemile D, et al. Parent's knowledge and perceptions of the health effects of environmental hazards in Sakarya, Turkey[J]. Journal of the Pakistan Medical Association, 2014, 64(1): 38-41.
[7] Kampa M, Castanas E. Human health effects of air pollution[J]. Environmental Pollution, 2008, 151(2): 362-368.
[8] Chen H, Goldberg M S, Villeneuve P J. A systematic review of the relation between long- term exposure to ambient air pollution and chronic diseases[J]. Reviews on Environmental Health, 2008, 23(4): 243-297.
[9] Liu L, Breitner S, Schneider A, et al. Size-fractioned particulate air pollution and cardiovascular emergency room visits in Beijing, China[J]. Environmental Research, 2013, 121: 52-63.
[10] Guo Y, Li S, Tian Z, et al. The burden of air pollution on years of life lost in Beijing, China, 2004-08: Retrospective regression analysis of daily deaths[J]. British Medical Journal, 2013, 347: f7139.
[11] Wang W, Lin P, Han C, et al. Vasculogenic mimicry contributes to lymph node metastasis of laryngeal squamous cell carcinoma[J]. Journal of Experimental & Clinical Cancer Research, 2010, 29: 60, doi: 10.1186/1756-9966-29-60.
[12] Liu R, Yang K, Meng C, et al. Vasculogenic mimicry is a marker of poor prognosis in prostate cancer[J]. Cancer Biology & Therapy, 2012, 13(7): 527-533.
[13] Kouassi K S, Billet S, Garcon G, et al. Oxidative damage induced in A549 cells by physically and chemically characterized air particulate matter (PM2.5) collected in Abidjan, Cote d'Ivoire[J]. Journal of Applied Toxicology, 2010, 30(4): 310-320.
[14] Ding X, Wang M, Chu H, et al. Global gene expression profiling of human bronchial epithelial cells exposed to airborne fine particulate matter collected from Wuhan, China[J]. Toxicology Letters, 2014, 228 (1): 25-33.
[15] Lund A K, Lucero J, Harman M, et al. The oxidized low- density lipoprotein receptor mediates vascular effects of inhaled vehicle emissions[J]. American Journal of Respiratory and Critical Care Medicine, 2011, 184(1): 82-91.
[16] Musah S, De Jarnett N, Hoyle G W. Tumor necrosis factor- alpha mediates interactions between macrophages and epithelial cells underlying proinflammatory gene expression induced by particulate matter[J]. Toxicology, 2012, 299(2-3): 125-132.
[17] Kuroda E, Coban C, Ishii K J. Particulate adjuvant and innate immunity: Past achievements, present findings, and future prospects[J]. International Reviews of Immunology, 2013, 32(2): 209-220.
[18] Carmeliet P, Jain R K. Molecular mechanisms and clinical applications of angiogenesis[J]. Nature, 2011, 473(7347): 298-307.
[19] Gomes F G, Nedel F, Alves A M, et al. Tumor angiogenesis and lymphangiogenesis: Tumor/endothelial crosstalk and cellular/microenvironmental signaling mechanisms[J]. Life Sciences, 2013, 92 (2): 101-107.
[20] Capdevila J, Carrato A, Tabernero J, et al. What could Nintedanib (BIBF 1120), a triple inhibitor of VEGFR, PDGFR, and FGFR, add to the current treatment options for patients with metastatic colorectal cancer?[J]. Critical Reviews in Oncology/Hematology, 2014, doi: 10.1016/j.critrevonc.2014.05.004.
[21] Styp- Rekowska B, Hlushchuk R, Pries A R, et al. Intussusceptive angiogenesis: Pillars against the blood flow[J]. Acta Physiologica (Oxford), 2011, 202(3): 213-223.
[22] Phinney D G, Prockop D J. Concise review: Mesenchymal stem/multipotent stromal cells: The state of transdifferentiation and modes of tissue repair- current views[J]. Stem Cells, 2007, 25(11): 2896- 2902.
[23] De Spiegelaere W, Casteleyn C, Van Den Broeck W, et al. Intussusceptive angiogenesis: A biologically relevant form of angiogenesis[J]. Journal of Vascular Research, 2012, 49(5): 390-404.
[24] Cao Z, Shang B, Zhang G, et al. Tumor cell-mediated neovascularization and lymphangiogenesis contrive tumor progression and cancer metastasis[J]. Biochimica et Biophysica Acta, 2013, 1836(2): 273-286.
[25] Kwon M J, Shin Y K. Regulation of ovarian cancer stem cells or tumor-initiating cells[J]. International Journal of Molecular Sciences, 2013, 14(4): 6624-6648.
[26] Dome B, Paku S, Somlai B, et al. Vascularization of cutaneous melanoma involves vessel cooption and has clinical significance[J]. The Journal of Pathology, 2002, 197(3): 355-362.
[27] Birrane G, Li H, Yang S, et al. Cigarette smoke induces nuclear translocation of heme oxygenase 1 (HO-1) in prostate cancer cells: nuclear HO-1 promotes vascular endothelial growth factor secretion[J]. International Journal of Oncology, 2013, 42(6): 1919-1928.
[28] Jazwa A, Loboda A, Golda S, et al. Effect of heme and heme oxygenase-1 on vascular endothelial growth factor synthesis and angiogenic potency of human keratinocytes[J]. Free radical Biology & Medicine, 2006, 40(7): 1250-1263.
[29] Chu Y K, Lee S C, Byeon S H. VEGF rescues cigarette smokinginduced human RPE cell death by increasing autophagic flux: Implications of the role of autophagy in advanced age-related macular degeneration[J]. Investigative Ophthalmology & Visual Science, 2013, 54(12): 7329-7337.
[30] Sugimoto A, Masuda H, Eguchi M, et al. Nicotine enlivenment of blood flow recovery following endothelial progenitor cell transplantation into ischemic hindlimb[J]. Stem Cells and Development, 2007, 16(4): 649-956.
[31] Ji K, Xing C, Jiang F, et al. Benzo [a] pyrene induces oxidative stress and endothelial progenitor cell dysfunction via the activation of the NF-kappaB pathway[J]. International Journal of Molecular Medicine, 2013, 31(4): 922-930.
[32] Hendrix M J, Seftor E A, Hess A R, et al. Vasculogenic mimicry and tumour- cell plasticity: Lessons from melanoma[J]. Nature Reviews Cancer, 2003, 3(6): 411-421.
[33] Warren G W, Singh A K. Nicotine and lung cancer[J]. Journal of Carcinogenesis, 2013, doi: 10.4103/1477-3163.
[34] Singh S, Pillai S, Chellappan S. Nicotinic acetylcholine receptor signaling in tumor growth and metastasis[J]. Journal of Oncology, 2011, 2011: 456743, doi: 10.1155/2011/456743.
[35] Warren G W, Romano M A, Kudrimoti M R, et al. Nicotinic modulation of therapeutic response in vitro and in vivo[J]. International Journal of Cancer, 2012, 131(11): 2519-2527.
[36] Masoumi M S, Amini A, Morris D L, et al. Significance of vascular endothelial growth factor in growth and peritoneal dissemination of ovarian cancer[J]. Cancer and Metastasis Reviews, 2012, 31(1-2): 143-162.
[37] Liu T J, Sun B C, Zhao X L, et al. CD133+ cells with cancer stem cell characteristics associates with vasculogenic mimicry in triplenegative breast cancer[J]. Oncogene, 2013, 32(5): 544-553.
[38] Ejaz S, Ejaz A, Sohail A, et al. Vascular and morphogenetic abnormalities associated with exposure of cigarette smoke condensate during chicken and murine embryogenesis[J]. Biomedical and Environmental Sciences, 2010, 23(4): 305-311.
[39] Ejaz S, Insan-ud-din, Ashraf M, et al. Cigarette smoke condensate and total particulate matter severely disrupts physiological angiogenesis[J]. Food and Chemical Toxicology, 2009, 47(3): 601-614.
[40] Acuner-Ozbabacan E, Engin B, Guven-Maiorov E, et al. The structural network of Interleukin- 10 and its implications in inflammation and cancer[J]. BMC Genomics, 2014, 15 (S4): S2.
[41] Pinato D J. Cancer- related inflammation: An emerging prognostic domain in metastatic castration-resistant prostate carcinoma[J]. Cancer, 2014, doi: 10.1002/cncr.28889.
[42] 杨凌, 马琼锦, 李莉珊, 等. PM2.5亚慢性染毒对小鼠肺部炎症及Th17/Treg的影响[J]. 卫生研究, 2014, 43(3): 387-392. Yang Ling, Ma Qiongjin, Li Lishan, et al. Effects of airborne fine particulate matters on pulmonary inflammation injury and Th17/Treg balance of sub-chronic exposure mice[J]. Wei Sheng Yan Jiu, 2014, 43(3): 387-392.
[43] Ding L, Li B, Zhao Y, et al. Serum CCL2 and CCL3 as potential biomarkers for the diagnosis of oral squamous cell carcinoma[J]. Tumour Biology, 2014, in press.
[44] Balamayooran G, Batra S, Cai S, et al. Role of CXCL5 in leukocyte recruitment to the lungs during secondhand smoke exposure[J]. American Journal of Respiratory Cell and Molecular Biology, 2012, 47 (1): 104-111.
[45] Mortaz E, Henricks P A, Kraneveld A D, et al. Cigarette smoke induces the release of CXCL-8 from human bronchial epithelial cells via TLRs and induction of the inflammasome[J]. Biochimica et Biophysica Acta, 2011, 1812(9): 1104-1110.
[46] Mierke C T. The fundamental role of mechanical properties in the progression of cancer disease and inflammation[J]. Reports on Progress in Physics, 2014, 77(7): 076602.
[47] Lee M S, Eum K D, Fang S C, et al. Oxidative stress and systemic inflammation as modifiers of cardiac autonomic responses to particulate air pollution[J]. International Journal of Cardiology, 2014, doi: 10.1016/j.ijcard.2014.07.012.
[48] Sreeja S, Geetha R, Priyadarshini E, et al. Substitution of soy protein for casein prevents oxidative modification and inflammatory response induced in rats fed high fructose diet[J]. ISRN Inflammation, 2014, 2014: 641096.
[49] Guo L, Li L, Wang W, et al. Mitochondrial reactive oxygen species mediates nicotine-induced hypoxia-inducible factor-1alpha expression in human non-small cell lung cancer cells[J]. Biochimica et Biophysica Acta, 2012, 1822(6): 852-861.
[50] Dewhirst M W, Cao Y, Moeller B. Cycling hypoxia and free radicals regulate angiogenesis and radiotherapy response[J]. Nature Reviews Cancer, 2008, 8(6): 425-437.
[51] Li Y, Ye D. Cancer therapy by targeting hypoxia-inducible factor-1[J]. Current Cancer Drug Targets, 2010, 10(7): 782-796.
[52] Sasaki H, Suzuki A, Shitara M, et al. Angiopoietin- like protein ANGPTL2 gene expression is correlated with lymph node metastasis in lung cancer[J]. Oncology letters, 2012, 4(6): 1325-1328.
[53] Huang R Y, Wong M K, Tan T Z, et al. An EMT spectrum defines an anoikis-resistant and spheroidogenic intermediate mesenchymal state that is sensitive to e-cadherin restoration by a src-kinase inhibitor, saracatinib (AZD0530)[J]. Cell Death & Disease, 2013, 4: e915.
[54] Liao G, Wang M, Ou Y, et al. IGF-1-induced epithelial-mesenchymal transition in MCF-7 cells is mediated by MUC1[J]. Cell Signal, 2014, 26(10): 2131-2137.
[55] Fantozzi A, Gruber D C, Pisarsky L, et al. VEGF-mediated angiogenesis links EMT- induced cancer stemness to tumor initiation[J]. Cancer Research, 2014, 74(5): 1566-1575.
[56] Xu M M, Mao G X, Liu J, et al. Low expression of the FoxO4 gene may contribute to the phenomenon of EMT in non- small cell lung cancer[J]. Asian Pacific Journal of Cancer Prevention, 2014, 15(9): 4013-4020.
[57] Shen H J, Sun Y H, Zhang S J, et al. Cigarette smoke- induced alveolarepithelial-mesenchymaltransitionismediatedbyRac1activation[J]. Biochimica et Biophysica Acta, 2014, 1840(6): 1838-1849.
[58] Ozaki K, Hori T, Ishibashi T, et al. Effects of chronic cigarette smoking on endothelial function in young men[J]. Journal of Cardiology, 2010, 56(3): 307-313.
[59] Lu Q, Sakhatskyy P, Grinnell K, et al. Cigarette smoke causes lung vascular barrier dysfunction via oxidative stress-mediated inhibition of RhoA and focal adhesion kinase[J]. American Journal of Physiology- lung Cellular and Molecular Physiology, 2011, 301(6): L847-857.
[60] Giannotta M, Trani M, Dejana E. VE- cadherin and endothelial adherens junctions: Active guardians of vascular integrity[J]. Developmental Cell, 2013, 26(5): 441-454.
[61] Oas R G, Nanes B A, Esimai C C, et al. p120-catenin and betacatenin differentially regulate cadherin adhesive function[J]. Molecular Biology of the Cell, 2013, 24(6): 704-714.
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