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中华普外科手术学杂志(电子版) ›› 2021, Vol. 15 ›› Issue (06) : 696 -699. doi: 10.3877/cma.j.issn.1674-3946.2021.06.031

综述

结直肠癌肝转移多阶段机制研究进展
李丁昌1, 曹李1, 陈鹏1, 董光龙1,()   
  1. 1. 100853 北京,解放军总医院第一医学中心普通外科医学部
  • 收稿日期:2021-02-07 出版日期:2021-12-26
  • 通信作者: 董光龙

Research progress on multi-stage mechanism of colorectal cancer liver metastasis

Dingchang Li1, Li Cao1, Peng Chen1, Guanglong Dong1,()   

  1. 1. Department of General Surgery, First Medical Center, General Hospital of PLA, Beijing 100853, China
  • Received:2021-02-07 Published:2021-12-26
  • Corresponding author: Guanglong Dong
  • Supported by:
    National Natural Science Foundation of China(81773247)
引用本文:

李丁昌, 曹李, 陈鹏, 董光龙. 结直肠癌肝转移多阶段机制研究进展[J/OL]. 中华普外科手术学杂志(电子版), 2021, 15(06): 696-699.

Dingchang Li, Li Cao, Peng Chen, Guanglong Dong. Research progress on multi-stage mechanism of colorectal cancer liver metastasis[J/OL]. Chinese Journal of Operative Procedures of General Surgery(Electronic Edition), 2021, 15(06): 696-699.

结直肠癌是我国常见恶性肿瘤类型之一,且很多患者在确诊时就已经发生了肝脏转移,这也是结直肠癌高死亡率的主要原因。因此研究结直肠癌肝转移(CLM)的机制具有重要意义。但目前肝转移具体机制尚不明确,本文将从细胞分子水平对肝转移的机制进行综述,期望为结直肠癌肝转移的研究治疗探索新的思路方法。

Colorectal cancer is one of the common types malignant tumor types in China, of malignant tumors in my country, and many patients have already experienced liver metastasis when they are diagnosed, which is also the main reason for the high mortality rate of colorectal cancer. Therefore, it is important to study the mechanism of colorectal cancer liver metastasis (CLM). However, the specific mechanism of liver metastasis is not clearstill unclear at present. This article will review the mechanism of liver metastasis from the cellular and molecular level, hoping to explore new ideas and methods for the research and treatment of colorectal cancer liver metastasis.

[1]
Siegel RL, Miller KD, Jemal A. Cancer statistics, 2019[J]. CA Cancer J Clin, 2019, 69(1): 7-34.
[2]
Jin M, Frankel WL. Lymph Node Metastasis in Colorectal Cancer[J]. Surg Oncol Clin N Am, 2018, 27(2): 401-412.
[3]
Van CUTSEM E, Cervantes A, Adam R, et al. ESMO consensus guidelines for the management of patients with metastatic colorectal cancer[J]. Ann Oncol, 2016, 27(8): 1386-1422.
[4]
Spano D, Zollo M. Tumor microenvironment: a main actor in the metastasis process[J]. Clin Exp Metastasis, 2012, 29(4): 381-395.
[5]
Arina A, Idel C, Hyjek EM, et al. Tumor-associated fibroblasts predominantly come from local and not circulating precursors[J]. Proc Natl Acad Sci USA, 2016, 113(27): 7551-7556.
[6]
Sahai E, Astsaturov I, Cukierman E, et al. A framework for advancing our understanding of cancer-associated fibroblasts[J]. Nat Rev Cancer, 2020, 20(3): 174-186.
[7]
Gaggioli C, Hooper S, Hidalgo-Carcedo C, et al. Fibroblast-led collective invasion of carcinoma cells with differing roles for RhoGTPases in leading and following cells[J]. Nat Cell Biol, 2007, 9(12): 1392-1400.
[8]
Hooper S, Gaggioli C, Sahai E. A chemical biology screen reveals a role for Rab21-mediated control of actomyosin contractility in fibroblast-driven cancer invasion[J]. Br J Cancer, 2010, 102(2): 392-402.
[9]
Calon A, Espinet E, Palomo-Ponce S, et al. Dependency of colorectal cancer on a TGF-beta-driven program in stromal cells for metastasis initiation[J]. Cancer Cell, 2012, 22(5): 571-584.
[10]
Calon A, Tauriello DV, Batlle E. TGF-beta in CAF-mediated tumor growth and metastasis[J]. Semin Cancer Biol, 2014, 25: 15-22.
[11]
Shi Y, Gao W, Lytle NK, et al. Targeting LIF-mediated paracrine interaction for pancreatic cancer therapy and monitoring[J]. Nature, 2019, 569(7754): 131-135.
[12]
Cazet AS, Hui MN, Elsworth BL, et al. Targeting stromal remodeling and cancer stem cell plasticity overcomes chemoresistance in triple negative breast cancer[J]. Nat Commun, 2018, 9(1): 2897.
[13]
Bruzzese F, Hagglof C, Leone A, et al. Local and systemic protumorigenic effects of cancer-associated fibroblast-derived GDF15[J]. Cancer Res, 2014, 74(13): 3408-3417.
[14]
Bhome R, Goh R, Pickard K, et al. Profiling the MicroRNA Payload of Exosomes Derived from Ex Vivo Primary Colorectal Fibroblasts[J]. Methods Mol Biol, 2017, 1509: 115-122.
[15]
Bhome R, Goh RW, Bullock MD, et al. Exosomal microRNAs derived from colorectal cancer-associated fibroblasts: role in driving cancer progression[J]. Aging (Albany NY), 2017, 9(12): 2666-2694.
[16]
Monteran L, Erez N. The Dark Side of Fibroblasts: Cancer-Associated Fibroblasts as Mediators of Immunosuppression in the Tumor Microenvironment[J]. Front Immunol, 2019, 10: 1835.
[17]
Sanford-Crane H, Abrego J, Sherman MH. Fibroblasts as Modulators of Local and Systemic Cancer Metabolism[J]. Cancers (Basel), 2019, 11(5): 619.
[18]
Bertero T, Oldham WM, Grasset EM, et al. Tumor-Stroma Mechanics Coordinate Amino Acid Availability to Sustain Tumor Growth and Malignancy[J]. Cell Metab, 2019, 29(1): 124-140.e10.
[19]
Liu R, Li J, Xie K, et al. FGFR4 promotes stroma-induced epithelial-to-mesenchymal transition in colorectal cancer[J]. Cancer Res, 2013, 73(19): 5926-5935.
[20]
Ozdemir BC, Pentcheva-Hoang T, Carstens JL, et al. Depletion of carcinoma-associated fibroblasts and fibrosis induces immunosuppression and accelerates pancreas cancer with reduced survival[J]. Cancer Cell, 2014, 25(6): 719-734.
[21]
Chanmee T, Ontong P, Konno K, et al. Tumor-associated macrophages as major players in the tumor microenvironment[J]. Cancers (Basel), 2014, 6(3): 1670-1690.
[22]
Kang JC, Chen JS, Lee CH, et al. Intratumoral macrophage counts correlate with tumor progression in colorectal cancer[J]. J Surg Oncol, 2010, 102(3): 242-248.
[23]
Wei C, Yang C, Wang S, et al. Crosstalk between cancer cells and tumor associated macrophages is required for mesenchymal circulating tumor cell-mediated colorectal cancer metastasis[J]. Mol Cancer, 2019, 18(1): 64.
[24]
Yang C, Wei C, Wang S, et al. Elevated CD163(+)/CD68(+) Ratio at Tumor Invasive Front is Closely Associated with Aggressive Phenotype and Poor Prognosis in Colorectal Cancer[J]. Int J Biol Sci, 2019, 15(5): 984-998.
[25]
Mantovani A, Cassatella MA, Costantini C, et al. Neutrophils in the activation and regulation of innate and adaptive immunity[J]. Nat Rev Immunol, 2011, 11(8): 519-531.
[26]
Fridlender ZG, Sun J, Kim S, et al. Polarization of tumor-associated neutrophil phenotype by TGF-beta: "N1" versus "N2" TAN[J]. Cancer Cell, 2009, 16(3): 183-194.
[27]
Houghton AM, Rzymkiewicz DM, Ji H, et al. Neutrophil elastase-mediated degradation of IRS-1 accelerates lung tumor growth[J]. Nat Med, 2010, 16(2): 219-223.
[28]
Kuang DM, Zhao Q, Wu Y, et al. Peritumoral neutrophils link inflammatory response to disease progression by fostering angiogenesis in hepatocellular carcinoma[J]. J Hepatol, 2011, 54(5): 948-955.
[29]
Wislez M, Rabbe N, Marchal J, et al. Hepatocyte growth factor production by neutrophils infiltrating bronchioloalveolar subtype pulmonary adenocarcinoma: role in tumor progression and death[J]. Cancer Res, 2003, 63(6): 1405-1412.
[30]
Hirai H, Fujishita T, Kurimoto K, et al. CCR1-mediated accumulation of myeloid cells in the liver microenvironment promoting mouse colon cancer metastasis[J]. Clin Exp Metastasis, 2014, 31(8): 977-989.
[31]
Itatani Y, Kawada K, Fujishita T, et al. Loss of SMAD4 from colorectal cancer cells promotes CCL15 expression to recruit CCR1+ myeloid cells and facilitate liver metastasis[J]. Gastroenterology, 2013, 145(5): 1064-1075.e11.
[32]
Yamamoto T, Kawada K, Itatani Y, et al. Loss of SMAD4 Promotes Lung Metastasis of Colorectal Cancer by Accumulation of CCR1+ Tumor-Associated Neutrophils through CCL15-CCR1 Axis[J]. Clin Cancer Res, 2017, 23(3): 833-844.
[33]
Pantel K, Speicher MR. The biology of circulating tumor cells[J]. Oncogene, 2016, 35(10): 1216-1224.
[34]
Aceto N, Bardia A, Miyamoto DT, et al. Circulating tumor cell clusters are oligoclonal precursors of breast cancer metastasis[J]. Cell, 2014, 158(5): 1110-1122.
[35]
Cheung KJ, Padmanaban V, Silvestri V, et al. Polyclonal breast cancer metastases arise from collective dissemination of keratin 14-expressing tumor cell clusters[J]. Proc Natl Acad Sci U S A, 2016, 113(7): E854-E863.
[36]
Liu X, Taftaf R, Kawaguchi M, et al. Homophilic CD44 Interactions Mediate Tumor Cell Aggregation and Polyclonal Metastasis in Patient-Derived Breast Cancer Models[J]. Cancer Discov, 2019, 9(1): 96-113.
[37]
Gkountela S, Castro-Giner F, Szczerba BM, et al. Circulating Tumor Cell Clustering Shapes DNA Methylation to Enable Metastasis Seeding[J]. Cell, 2019, 176(1-2): 98-112.e14.
[38]
Hou JM, Krebs M, Ward T, et al. Circulating tumor cells as a window on metastasis biology in lung cancer[J]. Am J Pathol, 2011, 178(3): 989-996.
[39]
Labelle M, Begum S, Hynes RO. Direct signaling between platelets and cancer cells induces an epithelial-mesenchymal-like transition and promotes metastasis[J]. Cancer Cell, 2011, 20(5): 576-590.
[40]
Aceto N, Toner M, Maheswaran S, et al. En Route to Metastasis: Circulating Tumor Cell Clusters and Epithelial-to-Mesenchymal Transition[J]. Trends Cancer, 2015, 1(1): 44-52.
[41]
Duda DG, Duyverman AM, Kohno M, et al. Malignant cells facilitate lung metastasis by bringing their own soil[J]. Proc Natl Acad Sci U S A, 2010, 107(50): 21677-21682.
[42]
Szczerba BM, Castro-Giner F, Vetter M, et al. Neutrophils escort circulating tumour cells to enable cell cycle progression[J]. Nature, 2019, 566(7745): 553-557.
[43]
Grillet F, Bayet E, Villeronce O, et al. Circulating tumour cells from patients with colorectal cancer have cancer stem cell hallmarks in ex vivo culture[J]. Gut, 2017, 66(10): 1802-1810.
[44]
Baek DH, Kim GH, Song GA, et al. Clinical Potential of Circulating Tumor Cells in Colorectal Cancer: A Prospective Study[J]. Clin Transl Gastroenterol, 2019, 10(7): e00055.
[45]
Arrazubi V, Mata E, Antelo ML, et al. Circulating Tumor Cells in Patients Undergoing Resection of Colorectal Cancer Liver Metastases. Clinical Utility for Long-Term Outcome: A Prospective Trial[J]. Ann Surg Oncol, 2019, 26(9): 2805-2811.
[46]
Kaplan RN, Riba RD, Zacharoulis S, et al. VEGFR1-positive haematopoietic bone marrow progenitors initiate the pre-metastatic niche[J]. Nature, 2005, 438(7069): 820-827.
[47]
Hoshino A, Costa-Silva B, Shen TL, et al. Tumour exosome integrins determine organotropic metastasis[J]. Nature, 2015, 527(7578): 329-335.
[48]
Costa-Silva B, Aiello NM, Ocean AJ, et al. Pancreatic cancer exosomes initiate pre-metastatic niche formation in the liver[J]. Nat Cell Biol, 2015, 17(6): 816-826.
[49]
Glinskii OV, Huxley VH, Glinsky GV, et al. Mechanical entrapment is insufficient and intercellular adhesion is essential for metastatic cell arrest in distant organs[J]. Neoplasia, 2005, 7(5): 522-527.
[50]
Hu CT, Guo LL, Feng N, et al. MIF, secreted by human hepatic sinusoidal endothelial cells, promotes chemotaxis and outgrowth of colorectal cancer in liver prometastasis[J]. Oncotarget, 2015, 6(26): 22410-22423.
[51]
Banerjee D, Hernandez SL, Garcia A, et al. Notch suppresses angiogenesis and progression of hepatic metastases[J]. Cancer Res, 2015, 75(8): 1592-1602.
[52]
Eveno C, Hainaud P, Rampanou A, et al. Proof of prometastatic niche induction by hepatic stellate cells[J]. J Surg Res, 2015, 194(2): 496-504.
[53]
Taura K, De Minicis S, Seki E, et al. Hepatic stellate cells secrete angiopoietin 1 that induces angiogenesis in liver fibrosis[J][J]. Gastroenterology, 2008, 135(5): 1729-1738.
[54]
Mook OR, Van Marle J, Jonges R, et al. Interactions between colon cancer cells and hepatocytes in rats in relation to metastasis[J]. J Cell Mol Med, 2008, 12(5b): 2052-2061.
[55]
Radinsky R, Risin S, Fan D, et al. Level and function of epidermal growth factor receptor predict the metastatic potential of human colon carcinoma cells[J]. Clin Cancer Res, 1995, 1(1): 19-31.
[56]
Tabaries S, Annis MG, Hsu BE, et al. Lyn modulates Claudin-2 expression and is a therapeutic target for breast cancer liver metastasis [J]. Oncotarget, 2015, 6(11): 9476-9487.
[57]
Cools-Lartigue J, Spicer J, Mcdonald B, et al. Neutrophil extracellular traps sequester circulating tumor cells and promote metastasis[J]. J Clin Invest, 2013, 123(8): 3446-3458.
[58]
Najmeh S, Cools-Lartigue J, Rayes RF, et al. Neutrophil extracellular traps sequester circulating tumor cells via beta1-integrin mediated interactions[J]. Int J Cancer, 2017, 140(10): 2321-2330.
[59]
albrengues j, shields ma, ng d, et al. Neutrophil extracellular traps produced during inflammation awaken dormant cancer cells in mice[J]. Science, 2018, 361(6409): eaao4227.
[60]
Yang L, Liu Q, Zhang X, et al. DNA of neutrophil extracellular traps promotes cancer metastasis via CCDC25[J]. Nature, 2020, 583(7814): 133-138.
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