国际口腔医学杂志 ›› 2020, Vol. 47 ›› Issue (1): 95-101.doi: 10.7518/gjkq.2020009

• 综述 • 上一篇    下一篇

骨微环境相关细胞对肿瘤细胞骨转移的作用及机制

曾刊,李鑫,汪成林,杨静,叶玲()   

  1. 口腔疾病研究国家重点实验室 国家口腔疾病临床医学研究中心 四川大学华西口腔医院牙体牙髓病科 成都 610041
  • 收稿日期:2019-05-21 修回日期:2019-09-21 出版日期:2020-01-01 发布日期:2020-01-01
  • 通讯作者: 叶玲
  • 作者简介:曾刊,硕士,Email: 1322499644@qq.com
  • 基金资助:
    国家自然科学基金(81771065)

Effects of bone microenvironment cells on tumor bone metastasis

Zeng Kan,Li Xin,Wang Chenglin,Yang Jing,Ye Ling()   

  1. State Key Laboratory of Oral Diseases & National Clinical Research Center for Oral Diseases & Dept. of Operative Dentistry and Endodontics, West China Hospital of Stomatology, Sichuan University, Chengdu 610041, China
  • Received:2019-05-21 Revised:2019-09-21 Online:2020-01-01 Published:2020-01-01
  • Contact: Ling Ye
  • Supported by:
    This study was supported by National Natural Science Foundation of China(81771065)

摘要:

肿瘤骨转移是肿瘤转移的重要组成部分。肿瘤骨转移的过程往往会经历肿瘤细胞的定植、休眠及活化等。从肿瘤细胞定植到骨微环境中,再到其休眠激活往往经历一段较长的潜伏期。肿瘤骨转移过程中,骨微环境中的成骨细胞、破骨细胞、骨髓基质细胞、免疫细胞及血管内皮细胞对肿瘤细胞的定植、休眠及活化过程有重要影响。在这个过程中,肿瘤细胞除自身调节外,还通过与骨微环境中的各种细胞发生相互作用。本文针对骨微环境中的相关细胞对肿瘤细胞骨转移的作用及机制研究的现状及进展作一综述。

关键词: 肿瘤骨转移, 骨微环境, 休眠, 定植, 扩增

Abstract:

Bone metastasis is an important part of tumor metastasis and includes colonization, dormancy, and proliferation. However, tumor cells undergo a long period of dormancy after colonization. Several cells, including osteoblast, osteoclast, marrow stromal cell, immune cell, and vascular endothelial cell, live in the bone microenvironment and contribute to the progress of bone metastasis. In addition to self-regulation, tumor cells interact with various cells in the bone microenvironment during metastasis. This study aims to analyze the effect of bone microenvironment cells on tumor bone metastasis and further explore such process.

Key words: bone metastasis, bone microenvironment, dormancy, colonization, proliferation

中图分类号: 

  • Q279
[1] Cetin K, Christiansen CF, Sværke C , et al. Survival in patients with breast cancer with bone metastasis: a Danish population-based cohort study on the pro-gnostic impact of initial stage of disease at breast cancer diagnosis and length of the bone metastasis-free interval[J]. BMJ Open, 2015,5(4):e007702.
[2] Uhr JW, Pantel K . Controversies in clinical cancer dormancy[J]. Proc Natl Acad Sci USA, 2011,108(30):12396-12400.
[3] 孟琳, 王丹丹, 唐琪 , 等. 肿瘤休眠及其相关机制研究进展[J]. 吉林大学学报(医学版), 2016,42(5):1030-1033.
Meng L, Wang DD, Tang Q , et al. Advanced research on tumor dormancy and its correlative mechanism[J]. J Jilin Univ (Med Ed), 2016,42(5):1030-1033.
[4] Croucher PI ,McDonald MM,Martin TJ. Bone metastasis: the importance of the neighbourhood[J]. Nat Rev Cancer, 2016,16(6):373-386.
[5] Quayle L, Ottewell PD, Holen I . Bone metastasis: molecular mechanisms implicated in tumour cell dormancy in breast and prostate cancer[J]. Curr Cancer Drug Targets, 2015,15(6):469-480.
[6] Monteiro AC, Leal AC, Gonçalves-Silva T , et al. T cells induce pre-metastatic osteolytic disease and help bone metastases establishment in a mouse mo-del of metastatic breast cancer[J]. PLoS One, 2013,8(7):e68171.
[7] Ghajar CM, Peinado H, Mori H , et al. The perivas-cular Niche regulates breast tumour dormancy[J]. Nat Cell Biol, 2013,15(7):807-817.
[8] Sosa MS, Bragado P, Aguirre-Ghiso JA . Mechanisms of disseminated cancer cell dormancy: an awakening field[J]. Nat Rev Cancer, 2014,14(9):611-622.
[9] Aguirre Ghiso JA . Inhibition of FAK signaling ac-tivated by urokinase receptor induces dormancy in human carcinoma cells in vivo[J]. Oncogene, 2002,21(16):2513-2524.
[10] Aguirre Ghiso JA, Kovalski K, Ossowski L . Tumor dormancy induced by downregulation of urokinase receptor in human carcinoma involves integrin and MAPK signaling[J]. J Cell Biol, 1999,147(1):89-104.
[11] Liu D, Aguirre Ghiso J, Estrada Y , et al. EGFR is a transducer of the urokinase receptor initiated signal that is required for in vivo growth of a human car-cinoma[J]. Cancer Cell, 2002,1(5):445-457.
[12] Aguirre-Ghiso JA, Ossowski L, Rosenbaum SK . Green fluorescent protein tagging of extracellular signal-regulated kinase and p38 pathways reveals novel dynamics of pathway activation during pri-mary and metastatic growth[J]. Cancer Res, 2004,64(20):7336-7345.
[13] Bartkowiak K, Effenberger KE, Harder S , et al. Discovery of a novel unfolded protein response phenotype of cancer stem/progenitor cells from the bone marrow of breast cancer patients[J]. J Proteome Res, 2010,9(6):3158-3168.
[14] Hosokawa N, Hara T, Kaizuka T , et al. Nutrient-dependent MTORC1 association with the ULK1-Atg13-FIP200 complex required for autophagy[J]. Mol Biol Cell, 2009,20(7):1981-1991.
[15] 张玉梅, 冯凡, 林方方 , 等. 自噬相关基因ATG5在肿瘤发生发展及治疗中的作用[J]. 中国肿瘤, 2018,27(10):774-778.
Zhang YM, Feng F, Lin FF , et al. Roles of auto-phagy-related gene 5 (ATG5) in tumor development, treatment and prognosis[J]. China Cancer, 2018,27(10):774-778.
[16] Malladi S, Macalinao DG, Jin X , et al. Metastatic latency and immune evasion through autocrine inhibition of WNT[J]. Cell, 2016,165(1):45-60.
[17] Zhuang XQ, Zhang H, Li XY , et al. Differential effects on lung and bone metastasis of breast cancer by Wnt signalling inhibitor DKK1[J]. Nat Cell Biol, 2017,19(10):1274-1285.
[18] Wang H, Yu CJ, Gao X , et al. The osteogenic Niche promotes early-stage bone colonization of disse-minated breast cancer cells[J]. Cancer Cell, 2015,27(2):193-210.
[19] Ren GW, Esposito M, Kang YB . Bone metastasis and the metastatic Niche[J]. J Mol Med, 2015,93(11):1203-1212.
[20] Buenrostro D, Park SI, Sterling JA . Dissecting the role of bone marrow stromal cells on bone metas-tases[J]. Biomed Res Int, 2014,2014:875305.
[21] Sun YN, Mao XY, Fan CF , et al. CXCL12-CXCR4 axis promotes the natural selection of breast cancer cell metastasis[J]. Tumor Biol, 2014,35(8):7765-7773.
[22] Luker KE, Lewin SA, Mihalko LA , et al. Scavenging of CXCL12 by CXCR7 promotes tumor growth and metastasis of CXCR4-positive breast cancer cells[J]. Oncogene, 2012,31(45):4750-4758.
[23] Boudot A, Kerdivel G, Habauzit D , et al. Differential estrogen-regulation of CXCL12 chemokine receptors, CXCR4 and CXCR7, contributes to the growth effect of estrogens in breast cancer cells[J]. PLoS One, 2011,6(6):e20898.
[24] Wang N, Docherty FE, Brown HK , et al. Prostate cancer cells preferentially home to osteoblast-rich areas in the early stages of bone metastasis: evidence from in vivo models[J]. J Bone Miner Res, 2014,29(12):2688-2696.
[25] Grudowska A, Czaplińska D, Polom W , et al. Tetras-panin CD151 mediates communication between PC3 prostate cancer cells and osteoblasts[J]. Acta Biochim Pol, 2017,64(1):135-141.
[26] Wang H, Tian L, Liu J , et al.The osteogenic Niche is a calcium reservoir of bone micrometastases and confers unexpected therapeutic vulnerability[J].Cancer Cell, 2018, 34(5):823- 839.e7.
[27] Weilbaecher KN, Guise TA , McCauley LK. Cancer to bone: a fatal attraction[J]. Nat Rev Cancer, 2011,11(6):411-425.
[28] Hirshberg A, Berger R, Allon I , et al. Metastatic tumors to the jaws and mouth[J]. Head Neck Pathol, 2014,8(4):463-474.
[29] Zheng Y, Chow SO, Boernert K , et al. Direct cross-talk between cancer and osteoblast lineage cells fuels metastatic growth in bone via auto-amplification of IL-6 and RANKL signaling pathways[J]. J Bone Miner Res, 2014,29(9):1938-1949.
[30] Luo XM, Fu YJ, Loza AJ , et al. Stromal-initiated changes in the bone promote metastatic niche deve-lopment[J]. Cell Rep, 2016,14(1):82-92.
[31] Esposito M, Guise T, Kang YB . The biology of bone metastasis[J]. Cold Spring Harb Perspect Med, 2018,8(6):a031252.
[32] Yin JJ, Selander K, Chirgwin JM , et al. TGF-beta signaling blockade inhibits PTHrP secretion by breast cancer cells and bone metastases development[J]. J Clin Invest, 1999,103(2):197-206.
[33] Lu X, Mu E, Wei Y , et al. VCAM-1 promotes osteolytic expansion of indolent bone micrometastasis of breast cancer by engaging α4β1-positive osteoclast pro-genitors[J]. Cancer Cell, 2011,20(6):701-714.
[34] Sethi N, Dai XD, Winter CG , et al. Tumor-derived JAGGED1 promotes osteolytic bone metastasis of breast cancer by engaging notch signaling in bone cells[J]. Cancer Cell, 2011,19(2):192-205.
[35] Lynch CC, Hikosaka A, Acuff HB , et al. MMP-7 promotes prostate cancer-induced osteolysis via the solubilization of RANKL[J]. Cancer Cell, 2005,7(5):485-496.
[36] Lu X, Wang QQ, Hu GH , et al. ADAMTS1 and MMP1 proteolytically engage EGF-like ligands in an osteolytic signaling cascade for bone metastasis[J]. Genes Dev, 2009,23(16):1882-1894.
[37] Kelly T, Suva LJ, Huang Y , et al. Expression of heparanase by primary breast tumors promotes bone resorption in the absence of detectable bone metas-tases[J]. Cancer Res, 2005,65(13):5778-5784.
[38] Cher ML, Biliran HR Jr, Bhagat S , et al. Maspin expression inhibits osteolysis, tumor growth, and angiogenesis in a model of prostate cancer bone metastasis[J]. Proc Natl Acad Sci U S A, 2003,100(13):7847-7852.
[39] Dormady SP, Zhang XM, Basch RS . Hematopoietic progenitor cells grow on 3T3 fibroblast monolayers that overexpress growth arrest-specific gene-6 (GAS6)[J]. Proc Natl Acad Sci U S A, 2000,97(22):12260-12265.
[40] Jung Y, Shiozawa Y, Wang JC , et al. Prevalence of prostate cancer metastases after intravenous inocula-tion provides clues into the molecular basis of dor-mancy in the bone marrow microenvironment[J]. Neoplasia, 2012,14(5):429-439.
[41] Shiozawa Y, Pedersen EA, Patel LR , et al. GAS6/AXL Axis regulates prostate cancer invasion, proli-feration, and survival in the bone marrow niche[J]. Neoplasia, 2010,12(2):116-127.
[42] Kobayashi A, Okuda H, Xing F , et al. Bone morpho-genetic protein 7 in dormancy and metastasis of prostate cancer stem-like cells in bone[J]. J Exp Med, 2011,208(13):2641-2655.
[43] Kim JK, Jung Y, Wang JC , et al. TBK1 regulates prostate cancer dormancy through mTOR inhibition[J]. Neoplasia, 2013,15(9):1064-1074.
[44] Feuerer M, Rocha M, Bai L , et al. Enrichment of memory T cells and other profound immunological changes in the bone marrow from untreated breast cancer patients[J]. Int J Cancer, 2001,92(1):96-105.
[45] Sawant A, Hensel JA, Chanda D , et al. Depletion of plasmacytoid dendritic cells inhibits tumor growth and prevents bone metastasis of breast cancer cells[J]. J Immunol, 2012,189(9):4258-4265.
[46] Wu AC, He YW, Broomfield A , et al. CD169+ ma-crophages mediate pathological formation of woven bone in skeletal lesions of prostate cancer[J]. J Pathol, 2016,239(2):218-230.
[47] Kianercy A, Pienta KJ . Positive feedback loops be-tween inflammatory, bone and cancer cells during metastatic niche construction[J]. Adv Exp Med Biol, 2016,936:137-148.
[48] Mulcrone PL, Campbell JP, Clément-Demange L , et al. Skeletal colonization by breast cancer cells is stimulated by an osteoblast and β2AR-dependent neo-angiogenic switch[J]. J Bone Miner Res, 2017,32(7):1442-1454.
[1] 李佩仪,张新春. 微环境酸碱度在组织工程骨再生中作用的研究进展[J]. 国际口腔医学杂志, 2021, 48(1): 64-70.
[2] 杜芹1,2 邹静1 李雨庆1 李明云1 周学东1. 健康儿童口腔微生物的定植[J]. 国际口腔医学杂志, 2016, 43(1): 57-.
[3] 满毅 吴庆庆 龚婷 宫苹. 美学区种植外科修复治疗流程新方案[J]. 国际口腔医学杂志, 2015, 42(4): 373-383.
[4] 杨晓琼1综述 邹静2审校. 低龄儿童龋与其相关致病菌的研究进展[J]. 国际口腔医学杂志, 2011, 38(4): 455-459.
[5] 张静兰综述 凌均棨审校. 福赛斯坦纳菌在感染根管内的定植和检测[J]. 国际口腔医学杂志, 2008, 35(3): 274-274~276.
[6] 刘劲松. 细菌在牙种植体表面的定植及影响因素[J]. 国际口腔医学杂志, 2004, 31(S1): -.
[7] 李颂. 变形链球菌的传播研究方法及影响因素研究进展[J]. 国际口腔医学杂志, 2002, 29(05): -.
[8] 陈舟,刘天佳. 变形链球菌群基因多态性的研究方法[J]. 国际口腔医学杂志, 2001, 28(01): -.
[9] 张为新. 细菌定植引导组织再生术屏障膜与牙周组织再生[J]. 国际口腔医学杂志, 1999, 26(04): -.
Viewed
Full text


Abstract

Cited

  Shared   
  Discussed   
[1] 张新春. 桩冠修复与无髓牙的保护[J]. 国际口腔医学杂志, 1999, 26(06): .
[2] 王昆润. 长期单侧鼻呼吸对头颅发育有不利影响[J]. 国际口腔医学杂志, 1999, 26(05): .
[3] 彭国光. 颈淋巴清扫术中颈交感神经干的解剖变异[J]. 国际口腔医学杂志, 1999, 26(05): .
[4] 杨凯. 淋巴化疗的药物运载系统及其应用现状[J]. 国际口腔医学杂志, 1999, 26(05): .
[5] 康非吾. 种植义齿下部结构生物力学研究进展[J]. 国际口腔医学杂志, 1999, 26(05): .
[6] 柴枫. 可摘局部义齿用Co-Cr合金的激光焊接[J]. 国际口腔医学杂志, 1999, 26(04): .
[7] 孟姝,吴亚菲,杨禾. 伴放线放线杆菌产生的细胞致死膨胀毒素及其与牙周病的关系[J]. 国际口腔医学杂志, 2005, 32(06): 458 -460 .
[8] 费晓露,丁一,徐屹. 牙周可疑致病菌对口腔黏膜上皮的粘附和侵入[J]. 国际口腔医学杂志, 2005, 32(06): 452 -454 .
[9] 赵兴福,黄晓晶. 变形链球菌蛋白组学研究进展[J]. 国际口腔医学杂志, 2008, 35(S1): .
[10] 庞莉苹,姚江武. 抛光和上釉对陶瓷表面粗糙度、挠曲强度及磨损性能的影响[J]. 国际口腔医学杂志, 2008, 35(S1): .