Research progress on mechanism of onset and development of colorectal cancer：From perspective of tumor niche_CHINESE JOURNAL OF BASES AND CLINICS IN GENERAL SURGERY

Authors：

张浩阳 ¹ ,  达明绪 ^1,2

1. The First Clinical College of Lanzhou University, Lanzhou 730000, P. R. China;
2. Department of Surgical Oncology, Gansu Provincial Hospital , Lanzhou 730000, P. R. China;

Corresponding author：

达明绪, Email: ldyy_damx@lzu.edu.cn

Keywords：

colorectal cancer; tumor niche; tumor cells; tumor microenvironment

DOI：

10.7507/1007-9424.202410005

Video：

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Abstract Full text Figures/Tables Video References Cited by

Objective To summarizes the mechanisms of carcinogenesis of colorectal cells, the occurrence and development of cancer cells, and their interactions with the tumor niche of colorectal cancer (CRC) from the perspective of the tumor niche, exploring new ideas for the prevention, diagnosis, and treatment of CRC. Method The relevant literature at home and abroad in recent years on the researches of mechanism of the occurrence and development of CRC and its relation with the tumor niche of CRC was searched and reviewed. Results The theory of tumor ecology indicates that the human normal body can be regarded as a relatively closed and perfect ecosystem. Each normal tissue and organ within the body represents a niche in this ecosystem, which interact, affect, and symbiotically coexist with each other, forming a dynamic ecological balance. Tumor cells, being a “new species” distinct from normal tissue cells, “invade” the ecological system of the normal body under specific conditions and interact with the surrounding microenvironment, which is defined as the tumor niche. Analysis of current literature retrieved from the perspective of the tumor niche suggested that although genetic factors are involved in the carcinogenesis of colorectal cells, the majority of such carcinogenesis stems from the continuous stimulation of the colorectal niche. Current research primarily focuses on the conclusion that the carcinogenesis of colorectal cells is associated with factors such as chronic inflammatory response, intestinal microorganisms, oxidative stress, and pyroptosis. After carcinogenesis and the eventual formation of colorectal cancer, the growth of cancer cells and tissues first requires breaching the defense of the immune system in the colorectal niche. Immune cells in the immune system play a crucial role in the tumor niche during the occurrence and development of CRC. Conclusions The proposal of the tumor niche concept enables researchers, when studying the mechanisms of tumor occurrence and development, to no longer merely focus on the tumor and its microenvironment. Instead, the tumor as a part of the body's ecosystem was studied. Components of the tumor niche, such as chronic inflammatory responses, intestinal microorganisms, oxidative stress, pyroptosis, and immune system, have a significant impact on the mechanisms of carcinogenesis of most colorectal cells, as well as the occurrence and development of cancer cells. These factors influence the progression of CRC in various aspects.

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1. 黄理宾, 黄秋实, 杨烈. 全球及中国的结直肠癌流行病学特征及防治: 2022《全球癌症统计报告》解读. 中国普外基础与临床杂志, 2024, 31(5): 530-537.
2. Xi Y, Xu P. Global colorectal cancer burden in 2020 and projections to 2040. Transl Oncol, 2021, 14(10): 101174. doi: 10.1016/j.tranon.2021.101174.
3. 郑荣寿, 陈茹, 韩冰峰, 等. 2022年中国恶性肿瘤流行情况分析. 中华肿瘤杂志, 2024, 46(3): 221-231.
4. 姚一菲, 孙可欣, 郑荣寿. 《2022全球癌症统计报告》解读: 中国与全球对比. 中国普外基础与临床杂志, 2024, 31(7): 769-780.
5. Whiteside TL. The tumor microenvironment and its role in promoting tumor growth. Oncogene, 2008, 27(45): 5904-5912.
6. Paget S. The distribution of secondary growths in cancer of the breast. Lancet, 1889, 133: 571-573.
7. Aasen T, Mesnil M, Naus CC, et al. Gap junctions and cancer: communicating for 50 years. Nat Rev Cancer, 2016, 16(12): 775-788.
8. Gonzalez H, Hagerling C, Werb Z. Roles of the immune system in cancer: from tumor initiation to metastatic progression. Genes Dev, 2018, 32(19-20): 1267-1284.
9. Zhao LY, Mei JX, Yu G, et al. Role of the gut microbiota in anticancer therapy: from molecular mechanisms to clinical applications. Signal Transduct Target Ther, 2023, 8(1): 201. doi: 10.1038/s41392-023-01406-7.
10. Atkin W, Wooldrage K, Parkin DM, et al. Long term effects of once-only flexible sigmoidoscopy screening after 17 years of follow-up: the UK Flexible Sigmoidoscopy Screening randomised controlled trial. Lancet, 2017, 389(10076): 1299-1311.
11. Cardoso R, Guo F, Heisser T, et al. Proportion and stage distribution of screen-detected and non-screen-detected colorectal cancer in nine European countries: an international, population-based study. Lancet Gastroenterol Hepatol, 2022, 7(8): 711-723.
12. Dal Buono A, Gaiani F, Poliani L, et al. Juvenile polyposis syndrome: An overview. Best Pract Res Clin Gastroenterol, 2022, 58-59: 101799. doi: 10.1016/j.bpg.2022.101799.
13. Kidambi TD, Kohli DR, Samadder NJ, et al. Hereditary polyposis syndromes. Curr Treat Options Gastroenterol, 2019, 17(4): 650-665.
14. Kim B, Won D, Jang M, et al. Next-generation sequencing with comprehensive bioinformatics analysis facilitates somatic mosaic APC gene mutation detection in patients with familial adenomatous polyposis. BMC Med Genomics, 2019, 12(1): 103. doi: 10.1186/s12920-019-0553-0.
15. Zhang Y, Meng Q, Sun Q, et al. LKB1 deficiency-induced metabolic reprogramming in tumorigenesis and non-neoplastic diseases. Mol Metab, 2021, 44: 101131. doi: 10.1016/j.molmet.2020.101131.
16. Yehia L, Keel E, Eng C. The clinical spectrum of PTEN mutations. Annu Rev Med, 2020, 71: 103-116.
17. Cerretelli G, Ager A, Arends MJ, et al. Molecular pathology of Lynch syndrome. J Pathol, 2020, 250(5): 518-531.
18. 周雄, 胡明, 蒋栋铭, 等. 结直肠癌进展相关关键分子事件研究进展. 肿瘤防治研究, 2023, 50(6): 609-615.
19. Vogelstein B, Papadopoulos N, Velculescu VE, et al. Cancer genome landscapes. Science, 2013, 339(6127): 1546-1558.
20. 康晓培, 郭振江, 刘防震. BAF57在结直肠癌组织中的表达及其对患者预后的影响. 癌变·畸变·突变, 2024, 36(5): 379-383.
21. Buniello A, MacArthur JAL, Cerezo M, et al. The NHGRI-EBI GWAS Catalog of published genome-wide association studies, targeted arrays and summary statistics 2019. Nucleic Acids Res, 2019, 47(D1): D1005-D1012. doi: 10.1093/nar/gky1120.
22. Peters JM, Gonzalez FJ. The evolution of carcinogenesis. Toxicol Sci, 2018, 165(2): 272-276.
23. Dekker E, Tanis PJ, Vleugels JLA, et al. Colorectal cancer. Lancet, 2019, 394(10207): 1467-1480.
24. Bell HN, Rebernick RJ, Goyert J, et al. Reuterin in the healthy gut microbiome suppresses colorectal cancer growth through altering redox balance. Cancer Cell, 2022, 40(2): 185-200.
25. De Matteis R, Flak MB, Gonzalez-Nunez M, et al. Aspirin activates resolution pathways to reprogram T cell and macrophage responses in colitis-associated colorectal cancer. Sci Adv, 2022, 8(5): eabl5420. doi: 10.1126/sciadv.abl5420.
26. Zhu M, Ma Z, Zhang X, et al. C-reactive protein and cancer risk: a pan-cancer study of prospective cohort and Mendelian randomization analysis. BMC Med, 2022, 20(1): 301. doi: 10.1186/s12916-022-02506-x.
27. 赖智勇, 胡嘉欣, 李枝键, 等. 基于单细胞质谱流式技术分析膀胱肿瘤微环境中免疫细胞的组成. 中国癌症防治杂志, 2020, 12(2): 169-174.
28. Nam JH, Noh GT, Chung SS, et al. Validity of C-reactive protein as a surrogate marker for infectious complications after surgery for colorectal cancer. Surg Infect (Larchmt), 2023, 24(5): 488-494.
29. 杨驰, 罗长江. 结直肠癌炎症、免疫及胆固醇代谢背景研究进展. 国际肿瘤学杂志, 2022, 49(10): 630-634.
30. Yin Y, Wan J, Yu J, et al. Molecular pathogenesis of colitis-associated colorectal cancer: immunity, genetics, and intestinal microecology. Inflamm Bowel Dis, 2023, 29(10): 1648-1657.
31. Hanahan D. Hallmarks of cancer: New dimensions. Cancer Discov, 2022, 12(1): 31-46.
32. Bosák J, Kohoutová D, Hrala M, et al. Escherichia coli from biopsies differ in virulence genes between patients with colorectal neoplasia and healthy controls. Front Microbiol, 2023, 14: 1141619. doi: 10.3389/fmicb.2023.1141619.
33. Li R, Jia Z, Trush MA. Defining ROS in biology and medicine. React Oxyg Species (Apex), 2016, 1(1): 9-21.
34. Valko M, Jomova K, Rhodes CJ, et al. Redox- and non-redox-metal-induced formation of free radicals and their role in human disease. Arch Toxicol, 2016, 90(1): 1-37.
35. Lin S, Li Y, Zamyatnin AA, et al. Reactive oxygen species and colorectal cancer. J Cell Physiol, 2018, 233(7): 5119-5132.
36. Hussain SP, Amstad P, Raja K, et al. Increased p53 mutation load in noncancerous colon tissue from ulcerative colitis: a cancer-prone chronic inflammatory disease. Cancer Res, 2000, 60(13): 3333-3337.
37. Neganova M, Liu J, Aleksandrova Y, et al. Therapeutic influence on important targets associated with chronic inflammation and oxidative stress in cancer treatment. Cancers (Basel), 2021, 13(23): 6062. doi: 10.3390/cancers13236062.
38. Xu P, Li F, Tang H. Pyroptosis and airway homeostasis regulation. Physiol Res, 2023, 72(1): 1-13.
39. Gong W, Shi Y, Ren J. Research progresses of molecular mechanism of pyroptosis and its related diseases. Immunobiology, 2020, 225(2): 151884. doi: 10.1016/j.imbio.2019.11.019.
40. Wei Y, Yang L, Pandeya A, et al. Pyroptosis-induced inflammation and tissue damage. J Mol Biol, 2022, 434(4): 167301. doi: 10.1016/j.jmb.2021.167301.
41. Liu Z, Wang C, Lin C. Pyroptosis as a double-edged sword: The pathogenic and therapeutic roles in inflammatory diseases and cancers. Life Sci, 2023, 318: 121498. doi: 10.1016/j.lfs.2023.121498.
42. Dubyak GR, Miller BA, Pearlman E. Pyroptosis in neutrophils: Multimodal integration of inflammasome and regulated cell death signaling pathways. Immunol Rev, 2023, 314(1): 229-249.
43. Lu L, Zhang Y, Tan X, et al. Emerging mechanisms of pyroptosis and its therapeutic strategy in cancer. Cell Death Discov, 2022, 8(1): 338. doi: 10.1038/s41420-022-01101-6.
44. Hu D, Cui L, Zhang S, et al. Antitumor effect of tubeimoside-Ⅰ on murine colorectal cancers through PKM2-dependent pyroptosis and immunomodulation. Naunyn Schmiedebergs Arch Pharmacol, 2024, 397(6): 4069-4087.
45. Chuang SY, Yang CH, Chou CC, et al. TLR-induced PAI-2 expression suppresses IL-1β processing via increasing autophagy and NLRP3 degradation. Proc Natl Acad Sci USA, 2013, 110(40): 16079-16084.
46. Guo W, Sun Y, Liu W, et al. Small molecule-driven mitophagy-mediated NLRP3 inflammasome inhibition is responsible for the prevention of colitis-associated cancer. Autophagy, 2014, 10(6): 972-985.
47. Zhao Y, Guo Q, Zhao K, et al. Small molecule GL-V9 protects against colitis-associated colorectal cancer by limiting NLRP3 inflammasome through autophagy. Oncoimmunology, 2017, 7(1): e1375640. doi: 10.1080/2162402X.2017.1375640.
48. Gazzillo A, Polidoro MA, Soldani C, et al. Relationship between epithelial-to-mesenchymal transition and tumor-associated macrophages in colorectal liver metastases. Int J Mol Sci, 2022, 23(24): 16197. doi: 10.3390/ijms232416197.
49. Fan T, Zhang M, Yang J, et al. Therapeutic cancer vaccines: advancements, challenges, and prospects. Signal Transduct Target Ther, 2023, 8(1): 450. doi: 10.1038/s41392-023-01674-3.
50. Allen-Vercoe E, Jobin C. Fusobacterium and enterobacteriaceae: important players for CRC?. Immunol Lett, 2014, 162(2 Pt A): 54-61.
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