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Open AccessOpen Access JUSTC Review 17 January 2024

Orchestration of the dynamic molecular and cellular society in cancer by intratumoral bacteria

  • 1.

    MOE Key Laboratory for Cellular Dynamics, Hefei National Research Center for Interdisciplinary Sciences at the Microscale, Hefei 230026, China

  • 2.

    Anhui Key Laboratory for Cellular Dynamics and Chemical Biology, University of Science and Technology of China, Hefei 230027, China

Cite this:
https://doi.org/10.52396/JUSTC-2022-0186
More Information
  • Author Bio:

    Rutian Zhong is an undergraduate student at the School of Earth and Space Sciences, University of Science and Technology of China. His current research focuses on cellular dynamics under the supervision of Prof. Xing Liu

    Xing Liu is a Professor of MOE Key Laboratory for Cellular Dynamics, University of Science and Technology of China (USTC). She received her Ph.D. degree in Cell Biology from USTC. Her research career has been dedicated to solving the key scientific questions and challenges of cell fate decision using chemical tools and methods

  • Corresponding author: E-mail: xing1017@ustc.edu.cn
  • Received Date: 18 January 2023
  • Accepted Date: 25 June 2023
    • Available Online: 17 January 2024
    Abstract

  • Abstract

    It has been a long-standing interest in the biomedical field to delineate pathogen‒host cell interactions. The latest advancements in single-cell analyses with multiomics approaches have begun to revolutionize our understanding of the impact of intratumoral bacteria on tumor development. Recent studies suggest that intratumoral bacteria modulate the communication between tumor cells and surrounding immune cells, which changes tumor progression and plasticity. Thus, a better understanding of the molecular mechanisms underlying intratumor bacteria-elicited pathogen‒host interactions will shed light on targeted interrogation in clinical oncology. This essay highlights recent progress in intratumor bacterial signaling and host cell plasticity control. In addition, we provide perspectives on how the molecular delineation of intratumor bacterial signaling and host cell plasticity control can help precision medicine and novel therapeutic development.

    Graphical abstract

    The emerging networks of intratumoral bacteria-cancer cell communication can be used as targets for precision interrogation of cancer progression.

    Abstract

    It has been a long-standing interest in the biomedical field to delineate pathogen‒host cell interactions. The latest advancements in single-cell analyses with multiomics approaches have begun to revolutionize our understanding of the impact of intratumoral bacteria on tumor development. Recent studies suggest that intratumoral bacteria modulate the communication between tumor cells and surrounding immune cells, which changes tumor progression and plasticity. Thus, a better understanding of the molecular mechanisms underlying intratumor bacteria-elicited pathogen‒host interactions will shed light on targeted interrogation in clinical oncology. This essay highlights recent progress in intratumor bacterial signaling and host cell plasticity control. In addition, we provide perspectives on how the molecular delineation of intratumor bacterial signaling and host cell plasticity control can help precision medicine and novel therapeutic development.

    • Public Summary

    • Intratumoral bacteria determine tumor progression and therapeutic efficacy.
    • Intratumoral bacteria interact with tumor cells and tumor-related immune cells.
    • Emerging evidence suggests that intratumoral bacteria-host cell interactions provide a unique niche for the precise interrogation of cancer progression.
    • A better understanding of intratumoral bacteria-host cell interactions would provide conceptual advancement in precision medicine.

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    • References(60)
  • [1]
    de Martel C, Ferlay J, Franceschi S, et al. Global burden of cancers attributable to infections in 2008: a review and synthetic analysis. The Lancet Oncology, 2012, 13 (6): 607–615. doi: 10.1016/S1470-2045(12)70137-7
    [2]
    Sfanos K S, Sauvageot J, Fedor H L, et al. A molecular analysis of prokaryotic and viral DNA sequences in prostate tissue from patients with prostate cancer indicates the presence of multiple and diverse microorganisms. The Prostate, 2008, 68 (3): 306–320. doi: 10.1002/pros.20680
    [3]
    Yao X, Smolka A J. Gastric parietal cell physiology and Helicobacter pylori –induced disease. Gastroenterology, 2019, 156 (8): 2158–2173. doi: 10.1053/j.gastro.2019.02.036
    [4]
    Nejman D, Livyatan I, Fuks G, et al. The human tumor microbiome is composed of tumor type-specific intracellular bacteria. Science, 2020, 368 (6494): 973–980. doi: 10.1126/science.aay9189
    [5]
    Fu A K, Yao B Q, Dong T T, et al. Tumor-resident intracellular microbiota promotes metastatic colonization in breast cancer. Cell, 2022, 185 (8): 1356–1372. doi: 10.1016/j.cell.2022.02.027
    [6]
    Longmore G D. Bacteria in tumors “hit the road” together. Cell, 2022, 185 (8): 1292–1294. doi: 10.1016/j.cell.2022.03.013
    [7]
    Garrett W S. Cancer and the microbiota. Science, 2015, 348 (6230): 80–86. doi: 10.1126/science.aaa4972
    [8]
    Chiu C Y. Viral pathogen discovery. Current Opinion in Microbiology, 2013, 16 (4): 468–478. doi: 10.1016/j.mib.2013.05.001
    [9]
    Parsonnet J. Bacterial infection as a cause of cancer. Environmental Health Perspectives, 1995, 103 (Suppl 8): 263–268. doi: 10.1289/ehp.95103s8263
    [10]
    IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Schistosomes, Liver Flukes and Helicobacter pylori. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, 1994 , 61: 177–240.
    [11]
    Payne R J H, Nowak M A, Blumberg B S. Analysis of a cellular model to account for the natural history of infection by the hepatitis B virus and its role in the development of primary hepatocellular carcinoma. Journal of Theoretical Biology, 1992, 159 (2): 215–240. doi: 10.1016/S0022-5193(05)80703-9
    [12]
    Rosin M P, El Din Zaki S S, Ward A J, et al. Involvement of inflammatory reactions and elevated cell proliferation in the development of bladder cancer in schistosomiasis patients. Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis, 1994, 305 (2): 283–292. doi: 10.1016/0027-5107(94)90248-8
    [13]
    Hirano S, Nakama R, Tamaki M, et al. Isolation and characterization of thirteen intestinal microorganisms capable of 7 alpha-dehydroxylating bile acids. Applied and Environmental Microbiology, 1981, 41 (3): 737–745. doi: 10.1128/aem.41.3.737-745.1981
    [14]
    Stadler J, Yeung K S, Furrer R, et al. Proliferative activity of rectal mucosa and soluble fecal bile acids in patients with normal colons and in patients with colonic polyps or cancer. Cancer Letters, 1988, 38 (3): 315–320. doi: 10.1016/0304-3835(88)90023-7
    [15]
    Hill M J. Bile acids and colorectal cancer: hypothesis. European Journal of Cancer Prevention, 1991, 1 (Suppl 2): 69–74. doi: 10.1097/00008469-199110002-00012
    [16]
    Baptista J, Bruce W R, Gupta I, et al. On distribution of different fecapentaenes, the fecal mutagens, in the human population. Cancer Letters, 1984, 22 (3): 299–303. doi: 10.1016/0304-3835(84)90166-6
    [17]
    Povey A C, Schiffman M, Taffe B G, et al. Laboratory and epidemiologic studies of fecapentaenes. Mutation Research, 1991, 259 (3/4): 387–397. doi: 10.1016/0165-1218(91)90129-a
    [18]
    Gupta I, Baptista J, Bruce W R, et al. Structures of fecapentaenes, the mutagens of bacterial origin isolated from human feces. Biochemistry, 1983, 22 (2): 241–245. doi: 10.1021/bi00271a001
    [19]
    Deschner E E, Ruperto J F, Lupton J R, et al. Dietary butyrate (tributyrin) does not enhance AOM-induced colon tumorigenesis. Cancer Letters, 1990, 52 (1): 79–82. doi: 10.1016/0304-3835(90)90080-H
    [20]
    Mcintyre A, Gibson P R, Young G P. Butyrate production from dietary fibre and protection against large bowel cancer in a rat model. Gut, 1993, 34 (3): 386–391. doi: 10.1136/gut.34.3.386
    [21]
    Yu T C, Guo F F, Yu Y N, et al. Fusobacterium nucleatum promotes chemoresistance to colorectal cancer by modulating autophagy. Cell, 2017, 170 (3): 548–563. doi: 10.1016/j.cell.2017.07.008
    [22]
    Geller L T, Barzily-Rokni M, Danino T, et al. Potential role of intratumor bacteria in mediating tumor resistance to the chemotherapeutic drug gemcitabine. Science, 2017, 357 (6356): 1156–1160. doi: 10.1126/science.aah5043
    [23]
    Hoption Cann S A, van Netten J P, van Netten C. Dr William Coley and tumour regression: a place in history or in the future. Postgraduate Medical Journal, 2003, 79 (938): 672–680. doi: 10.1093/postgradmedj/79.938.672
    [24]
    Mager D L. Bacteria and cancer: cause, coincidence or cure? A review. Journal of translational medicine, 2006, 4 (1): 14. doi: 10.1186/1479-5876-4-14
    [25]
    de Jong R, Altare F, Haagen I A, et al. Severe mycobacterial and Salmonella infections in interleukin-12 receptor-deficient patients. Science, 1998, 280 (5368): 1435–1438. doi: 10.1126/science.280.5368.1435
    [26]
    Flemer B, Lynch D B, Brown J M R, et al. Tumour-associated and non-tumour-associated microbiota in colorectal cancer. Gut, 2017, 66 (4): 633–643. doi: 10.1136/gutjnl-2015-309595
    [27]
    Haggar F A, Boushey R P. Colorectal cancer epidemiology: incidence, mortality, survival, and risk factors. Clinics in Colon and Rectal Surgery, 2009, 22 (4): 191–197. doi: 10.1055/s-0029-1242458
    [28]
    Zackular J P, Rogers M A M, Ruffin M T, et al. The human gut microbiome as a screening tool for colorectal cancer. Cancer Prevention Research, 2014, 7 (11): 1112–1121. doi: 10.1158/1940-6207.CAPR-14-0129
    [29]
    Yu J, Feng Q, Wong S H, et al. Metagenomic analysis of faecal microbiome as a tool towards targeted non-invasive biomarkers for colorectal cancer. Gut, 2017, 66 (1): 70–78. doi: 10.1136/gutjnl-2015-309800
    [30]
    Zeller G, Tap J, Voigt A Y, et al. Potential of fecal microbiota for early-stage detection of colorectal cancer. Molecular Systems Biology, 2014, 10 (11): 766. doi: 10.15252/msb.20145645
    [31]
    Galeano Niño J L, Wu H, LaCourse K D, et al. Effect of the intratumoral microbiota on spatial and cellular heterogeneity in cancer. Nature, 2022, 611 (7937): 810–817. doi: 10.1038/s41586-022-05435-0
    [32]
    Provenzano P P, Eliceiri K W, Campbell J M, et al. Collagen reorganization at the tumor-stromal interface facilitates local invasion. BMC Medicine, 2006, 4 (1): 38. doi: 10.1186/1741-7015-4-38
    [33]
    Conklin M W, Eickhoff J C, Riching K M, et al. Aligned collagen is a prognostic signature for survival in human breast carcinoma. The American Journal of Pathology, 2011, 178 (3): 1221–1232. doi: 10.1016/j.ajpath.2010.11.076
    [34]
    Ingman W V, Wyckoff J, Gouon-Evans V, et al. Macrophages promote collagen fibrillogenesis around terminal end buds of the developing mammary gland. Developmental Dynamics, 2006, 235 (12): 3222–3229. doi: 10.1002/dvdy.20972
    [35]
    Leek R D, Harris A L. Tumor-associated macrophages in breast cancer. Journal of Mammary Gland Biology and Neoplasia, 2002, 7 (2): 177–189. doi: 10.1023/A:1020304003704
    [36]
    Chen J Q, Yao Y D, Gong C, et al. CCL18 from tumor-associated macrophages promotes breast cancer metastasis via PITPNM3. Cancer Cell, 2011, 19 (4): 541–555. doi: 10.1016/j.ccr.2011.02.006
    [37]
    Xu H X, Lyu X D, Yi M, et al. Organoid technology and applications in cancer research. Journal of Hematology & Oncology, 2018, 11 (1): 116. doi: 10.1186/s13045-018-0662-9
    [38]
    Ness R B, Cauley J A. Antibiotics and breast cancer—what’s the meaning of this? JAMA, 2004, 291 (7): 880–881. doi: 10.1001/jama.291.7.880
    [39]
    Rao V P, Poutahidis T, Fox J G, et al. Breast cancer: should gastrointestinal bacteria be on our radar screen? Cancer Research, 2007, 67 (3): 847–850. doi: 10.1158/0008-5472.CAN-06-3468
    [40]
    Kalaora S, Nagler A, Nejman D, et al. Identification of bacteria-derived HLA-bound peptides in melanoma. Nature, 2021, 592 (7852): 138–143. doi: 10.1038/s41586-021-03368-8
    [41]
    Strobel M, Pförtner H, Tuchscherr L, et al. Post-invasion events after infection with Staphylococcus aureus are strongly dependent on both the host cell type and the infecting S. aureus strain. Clinical Microbiology and Infection, 2016, 22 (9): 799–809. doi: 10.1016/j.cmi.2016.06.020
    [42]
    Urbaniak C, Gloor G B, Brackstone M, et al. The microbiota of breast tissue and its association with breast cancer. Applied and Environmental Microbiology, 2016, 82 (16): 5039–5048. doi: 10.1128/AEM.01235-16
    [43]
    Buc E, Dubois D, Sauvanet P, et al. High prevalence of mucosa-associated E. coli producing cyclomodulin and genotoxin in colon cancer. PLoS ONE, 2013, 8 (2): e56964. doi: 10.1371/journal.pone.0056964
    [44]
    Cuevas-Ramos G, Petit C R, Marcq I, et al. Escherichia coli induces DNA damage in vivo and triggers genomic instability in mammalian cells. Proceedings of the National Academy of Sciences of the United States of America, 2010, 107 (25): 11537–11542. doi: 10.1073/pnas.1001261107
    [45]
    Arthur J C, Perez-Chanona E, Mühlbauer M, et al. Intestinal inflammation targets cancer-inducing activity of the microbiota. Science, 2012, 338 (6103): 120–123. doi: 10.1126/science.1224820
    [46]
    Nougayrède J P, Homburg S, Taieb F, et al. Escherichia coli induces DNA double-strand breaks in eukaryotic cells. Science, 2006, 313 (5788): 848–851. doi: 10.1126/science.1127059
    [47]
    Fernández M F, Reina-Pérez I, Astorga J M, et al. Breast cancer and its relationship with the microbiota. International Journal of Environmental Research and Public Health, 2018, 15 (8): 1747. doi: 10.3390/ijerph15081747
    [48]
    Hieken T J, Chen J, Hoskin T L, et al. The microbiome of aseptically collected human breast tissue in benign and malignant disease. Scientific Reports, 2016, 6 (1): 30751. doi: 10.1038/srep30751
    [49]
    Xue T, Lu Y, Yang H, et al. Isothermal RNA amplification for the detection of viable pathogenic bacteria to estimate the Salmonella virulence for causing enteritis. Journal of Agricultural and Food Chemistry, 2022, 70 (5): 1670–1678. doi: 10.1021/acs.jafc.1c07182
    [50]
    Urbaniak C, Cummins J, Brackstone M, et al. Microbiota of human breast tissue. Applied and Environmental Microbiology, 2014, 80 (10): 3007–3014. doi: 10.1128/AEM.00242-14
    [51]
    Thompson K J, Ingle J N, Tang X, et al. A comprehensive analysis of breast cancer microbiota and host gene expression. PLoS ONE, 2017, 12 (11): e0188873. doi: 10.1371/journal.pone.0188873
    [52]
    Ghoncheh M, Pournamdar Z, Salehiniya H. Incidence and mortality and epidemiology of breast cancer in the world. Asian Pacific Journal of Cancer Prevention, 2016, 17 (sup3): 43–46. doi: 10.7314/APJCP.2016.17.S3.43
    [53]
    Soto A M, Sonnenschein C. Environmental causes of cancer: endocrine disruptors as carcinogens. Nature Reviews Endocrinology, 2010, 6 (7): 363–370. doi: 10.1038/nrendo.2010.87
    [54]
    Goering P L, Aposhian H V, Mass M J, et al. The enigma of arsenic carcinogenesis: role of metabolism. Toxicological Sciences, 1999, 49 (1): 5–14. doi: 10.1093/toxsci/49.1.5
    [55]
    Sorahan T, Harrington J M. Lung cancer in Yorkshire chrome platers, 1972–97. Occupational & Environmental Medicine, 2000, 57 (6): 385–389. doi: 10.1136/oem.57.6.385
    [56]
    Lei Y X, Chen X M, Chen J K. Antisense translation elongation factor TEF_1δ reverses the carcinogenicity of cadmium chloride. Carcinogenesis, Teratogenesis and Mutagenesis, 2005, 17 (1): 1–4.
    [57]
    Liu X, Liu X, Wang H, et al. Phase separation drives decision making in cell division. Journal of Biological Chemistry, 2020, 295 (39): 13419–13431. doi: 10.1074/jbc.REV120.011746
    [58]
    Wang W, Yang F, Lin J, et al. Modeling of COVID-19 disease disparity in gastric organoids reveals the spatiotemporal dynamics of SARS-CoV-2 infectivity. Journal of Molecular Cell Biology, 2022, 14 (2): mjac007. doi: 10.1093/jmcb/mjac007
    [59]
    Poore G D, Kopylova E, Zhu Q, et al. Microbiome analyses of blood and tissues suggest cancer diagnostic approach. Nature, 2020, 579 (7800): 567–574. doi: 10.1038/s41586-020-2095-1
    [60]
    Gurbatri C R, Arpaia N, Danino T. Engineering bacteria as interactive cancer therapies. Science, 2022, 378 (6622): 858–864. doi: 10.1126/science.add9667
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    Figure  1.  Three modes of how bacteria weaken cancer. (a) Bacterial colonization can lower the risk of certain cancers by either impeding the production of cancer cells or occupying the space where tumors typically grow. (b) If bacterial colonization is absent, ample space and nutrition could be available for cancer cells to thrive. (c) Either the bacteria themselves or their toxins have the ability to affect cancer cells, potentially eliminating or weakening them.

    Figure  2.  A hypothetical model of bacterium-induced breast cancer. Breast cancer in mice occurs from infection with H. hepaticus bacteria that stem from mammary ducts, inflammatory foci and proliferative epithelium of ducts. The spectrum of morphological intermediates from normal breast tissue (A) to precancerous (B and C) and tumor (D) states are shown: ductal hyperplasia (B) with focal alveolar hyperplasia (B, insets), early adenosquamous metaplasia (C) with ductal carcinoma in situ (breast intraepithelial neoplasia) and apocrine cytoplasmic differentiation (C, insets), and finally adenocarcinoma (D). H&E staining. Magnification, 40× (A–D); 400× (insets). Adapted with permission from Ref. [39]. Copyright 2007, American Association for Cancer Research.

    Figure  3.  Bacterial specificity in certain tumor types. The green circle signifies that these bacteria have a noticeable enrichment in certain tumor types. By examining the list, it is apparent that breast cancer cells harbor significantly more diverse bacterial species than other tumors, suggesting that they could be suitable candidates for studying intratumoral bacteria. It only highlights the specificity of bacterial species and does not indicate their prevalence in the original article.

    Figure  4.  A representative model of bacterial entry into host cells using 3D organoids. Molecular delineation of primary and secondary infection could offer a novel niche to learn about virus‒host interactions for disease disparity and severity. Adapted from Ref. [58]. Copyright 2022, The Author(s).

    [1]
    de Martel C, Ferlay J, Franceschi S, et al. Global burden of cancers attributable to infections in 2008: a review and synthetic analysis. The Lancet Oncology, 2012, 13 (6): 607–615. doi: 10.1016/S1470-2045(12)70137-7
    [2]
    Sfanos K S, Sauvageot J, Fedor H L, et al. A molecular analysis of prokaryotic and viral DNA sequences in prostate tissue from patients with prostate cancer indicates the presence of multiple and diverse microorganisms. The Prostate, 2008, 68 (3): 306–320. doi: 10.1002/pros.20680
    [3]
    Yao X, Smolka A J. Gastric parietal cell physiology and Helicobacter pylori –induced disease. Gastroenterology, 2019, 156 (8): 2158–2173. doi: 10.1053/j.gastro.2019.02.036
    [4]
    Nejman D, Livyatan I, Fuks G, et al. The human tumor microbiome is composed of tumor type-specific intracellular bacteria. Science, 2020, 368 (6494): 973–980. doi: 10.1126/science.aay9189
    [5]
    Fu A K, Yao B Q, Dong T T, et al. Tumor-resident intracellular microbiota promotes metastatic colonization in breast cancer. Cell, 2022, 185 (8): 1356–1372. doi: 10.1016/j.cell.2022.02.027
    [6]
    Longmore G D. Bacteria in tumors “hit the road” together. Cell, 2022, 185 (8): 1292–1294. doi: 10.1016/j.cell.2022.03.013
    [7]
    Garrett W S. Cancer and the microbiota. Science, 2015, 348 (6230): 80–86. doi: 10.1126/science.aaa4972
    [8]
    Chiu C Y. Viral pathogen discovery. Current Opinion in Microbiology, 2013, 16 (4): 468–478. doi: 10.1016/j.mib.2013.05.001
    [9]
    Parsonnet J. Bacterial infection as a cause of cancer. Environmental Health Perspectives, 1995, 103 (Suppl 8): 263–268. doi: 10.1289/ehp.95103s8263
    [10]
    IARC Working Group on the Evaluation of Carcinogenic Risks to Humans. Schistosomes, Liver Flukes and Helicobacter pylori. IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, 1994 , 61: 177–240.
    [11]
    Payne R J H, Nowak M A, Blumberg B S. Analysis of a cellular model to account for the natural history of infection by the hepatitis B virus and its role in the development of primary hepatocellular carcinoma. Journal of Theoretical Biology, 1992, 159 (2): 215–240. doi: 10.1016/S0022-5193(05)80703-9
    [12]
    Rosin M P, El Din Zaki S S, Ward A J, et al. Involvement of inflammatory reactions and elevated cell proliferation in the development of bladder cancer in schistosomiasis patients. Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis, 1994, 305 (2): 283–292. doi: 10.1016/0027-5107(94)90248-8
    [13]
    Hirano S, Nakama R, Tamaki M, et al. Isolation and characterization of thirteen intestinal microorganisms capable of 7 alpha-dehydroxylating bile acids. Applied and Environmental Microbiology, 1981, 41 (3): 737–745. doi: 10.1128/aem.41.3.737-745.1981
    [14]
    Stadler J, Yeung K S, Furrer R, et al. Proliferative activity of rectal mucosa and soluble fecal bile acids in patients with normal colons and in patients with colonic polyps or cancer. Cancer Letters, 1988, 38 (3): 315–320. doi: 10.1016/0304-3835(88)90023-7
    [15]
    Hill M J. Bile acids and colorectal cancer: hypothesis. European Journal of Cancer Prevention, 1991, 1 (Suppl 2): 69–74. doi: 10.1097/00008469-199110002-00012
    [16]
    Baptista J, Bruce W R, Gupta I, et al. On distribution of different fecapentaenes, the fecal mutagens, in the human population. Cancer Letters, 1984, 22 (3): 299–303. doi: 10.1016/0304-3835(84)90166-6
    [17]
    Povey A C, Schiffman M, Taffe B G, et al. Laboratory and epidemiologic studies of fecapentaenes. Mutation Research, 1991, 259 (3/4): 387–397. doi: 10.1016/0165-1218(91)90129-a
    [18]
    Gupta I, Baptista J, Bruce W R, et al. Structures of fecapentaenes, the mutagens of bacterial origin isolated from human feces. Biochemistry, 1983, 22 (2): 241–245. doi: 10.1021/bi00271a001
    [19]
    Deschner E E, Ruperto J F, Lupton J R, et al. Dietary butyrate (tributyrin) does not enhance AOM-induced colon tumorigenesis. Cancer Letters, 1990, 52 (1): 79–82. doi: 10.1016/0304-3835(90)90080-H
    [20]
    Mcintyre A, Gibson P R, Young G P. Butyrate production from dietary fibre and protection against large bowel cancer in a rat model. Gut, 1993, 34 (3): 386–391. doi: 10.1136/gut.34.3.386
    [21]
    Yu T C, Guo F F, Yu Y N, et al. Fusobacterium nucleatum promotes chemoresistance to colorectal cancer by modulating autophagy. Cell, 2017, 170 (3): 548–563. doi: 10.1016/j.cell.2017.07.008
    [22]
    Geller L T, Barzily-Rokni M, Danino T, et al. Potential role of intratumor bacteria in mediating tumor resistance to the chemotherapeutic drug gemcitabine. Science, 2017, 357 (6356): 1156–1160. doi: 10.1126/science.aah5043
    [23]
    Hoption Cann S A, van Netten J P, van Netten C. Dr William Coley and tumour regression: a place in history or in the future. Postgraduate Medical Journal, 2003, 79 (938): 672–680. doi: 10.1093/postgradmedj/79.938.672
    [24]
    Mager D L. Bacteria and cancer: cause, coincidence or cure? A review. Journal of translational medicine, 2006, 4 (1): 14. doi: 10.1186/1479-5876-4-14
    [25]
    de Jong R, Altare F, Haagen I A, et al. Severe mycobacterial and Salmonella infections in interleukin-12 receptor-deficient patients. Science, 1998, 280 (5368): 1435–1438. doi: 10.1126/science.280.5368.1435
    [26]
    Flemer B, Lynch D B, Brown J M R, et al. Tumour-associated and non-tumour-associated microbiota in colorectal cancer. Gut, 2017, 66 (4): 633–643. doi: 10.1136/gutjnl-2015-309595
    [27]
    Haggar F A, Boushey R P. Colorectal cancer epidemiology: incidence, mortality, survival, and risk factors. Clinics in Colon and Rectal Surgery, 2009, 22 (4): 191–197. doi: 10.1055/s-0029-1242458
    [28]
    Zackular J P, Rogers M A M, Ruffin M T, et al. The human gut microbiome as a screening tool for colorectal cancer. Cancer Prevention Research, 2014, 7 (11): 1112–1121. doi: 10.1158/1940-6207.CAPR-14-0129
    [29]
    Yu J, Feng Q, Wong S H, et al. Metagenomic analysis of faecal microbiome as a tool towards targeted non-invasive biomarkers for colorectal cancer. Gut, 2017, 66 (1): 70–78. doi: 10.1136/gutjnl-2015-309800
    [30]
    Zeller G, Tap J, Voigt A Y, et al. Potential of fecal microbiota for early-stage detection of colorectal cancer. Molecular Systems Biology, 2014, 10 (11): 766. doi: 10.15252/msb.20145645
    [31]
    Galeano Niño J L, Wu H, LaCourse K D, et al. Effect of the intratumoral microbiota on spatial and cellular heterogeneity in cancer. Nature, 2022, 611 (7937): 810–817. doi: 10.1038/s41586-022-05435-0
    [32]
    Provenzano P P, Eliceiri K W, Campbell J M, et al. Collagen reorganization at the tumor-stromal interface facilitates local invasion. BMC Medicine, 2006, 4 (1): 38. doi: 10.1186/1741-7015-4-38
    [33]
    Conklin M W, Eickhoff J C, Riching K M, et al. Aligned collagen is a prognostic signature for survival in human breast carcinoma. The American Journal of Pathology, 2011, 178 (3): 1221–1232. doi: 10.1016/j.ajpath.2010.11.076
    [34]
    Ingman W V, Wyckoff J, Gouon-Evans V, et al. Macrophages promote collagen fibrillogenesis around terminal end buds of the developing mammary gland. Developmental Dynamics, 2006, 235 (12): 3222–3229. doi: 10.1002/dvdy.20972
    [35]
    Leek R D, Harris A L. Tumor-associated macrophages in breast cancer. Journal of Mammary Gland Biology and Neoplasia, 2002, 7 (2): 177–189. doi: 10.1023/A:1020304003704
    [36]
    Chen J Q, Yao Y D, Gong C, et al. CCL18 from tumor-associated macrophages promotes breast cancer metastasis via PITPNM3. Cancer Cell, 2011, 19 (4): 541–555. doi: 10.1016/j.ccr.2011.02.006
    [37]
    Xu H X, Lyu X D, Yi M, et al. Organoid technology and applications in cancer research. Journal of Hematology & Oncology, 2018, 11 (1): 116. doi: 10.1186/s13045-018-0662-9
    [38]
    Ness R B, Cauley J A. Antibiotics and breast cancer—what’s the meaning of this? JAMA, 2004, 291 (7): 880–881. doi: 10.1001/jama.291.7.880
    [39]
    Rao V P, Poutahidis T, Fox J G, et al. Breast cancer: should gastrointestinal bacteria be on our radar screen? Cancer Research, 2007, 67 (3): 847–850. doi: 10.1158/0008-5472.CAN-06-3468
    [40]
    Kalaora S, Nagler A, Nejman D, et al. Identification of bacteria-derived HLA-bound peptides in melanoma. Nature, 2021, 592 (7852): 138–143. doi: 10.1038/s41586-021-03368-8
    [41]
    Strobel M, Pförtner H, Tuchscherr L, et al. Post-invasion events after infection with Staphylococcus aureus are strongly dependent on both the host cell type and the infecting S. aureus strain. Clinical Microbiology and Infection, 2016, 22 (9): 799–809. doi: 10.1016/j.cmi.2016.06.020
    [42]
    Urbaniak C, Gloor G B, Brackstone M, et al. The microbiota of breast tissue and its association with breast cancer. Applied and Environmental Microbiology, 2016, 82 (16): 5039–5048. doi: 10.1128/AEM.01235-16
    [43]
    Buc E, Dubois D, Sauvanet P, et al. High prevalence of mucosa-associated E. coli producing cyclomodulin and genotoxin in colon cancer. PLoS ONE, 2013, 8 (2): e56964. doi: 10.1371/journal.pone.0056964
    [44]
    Cuevas-Ramos G, Petit C R, Marcq I, et al. Escherichia coli induces DNA damage in vivo and triggers genomic instability in mammalian cells. Proceedings of the National Academy of Sciences of the United States of America, 2010, 107 (25): 11537–11542. doi: 10.1073/pnas.1001261107
    [45]
    Arthur J C, Perez-Chanona E, Mühlbauer M, et al. Intestinal inflammation targets cancer-inducing activity of the microbiota. Science, 2012, 338 (6103): 120–123. doi: 10.1126/science.1224820
    [46]
    Nougayrède J P, Homburg S, Taieb F, et al. Escherichia coli induces DNA double-strand breaks in eukaryotic cells. Science, 2006, 313 (5788): 848–851. doi: 10.1126/science.1127059
    [47]
    Fernández M F, Reina-Pérez I, Astorga J M, et al. Breast cancer and its relationship with the microbiota. International Journal of Environmental Research and Public Health, 2018, 15 (8): 1747. doi: 10.3390/ijerph15081747
    [48]
    Hieken T J, Chen J, Hoskin T L, et al. The microbiome of aseptically collected human breast tissue in benign and malignant disease. Scientific Reports, 2016, 6 (1): 30751. doi: 10.1038/srep30751
    [49]
    Xue T, Lu Y, Yang H, et al. Isothermal RNA amplification for the detection of viable pathogenic bacteria to estimate the Salmonella virulence for causing enteritis. Journal of Agricultural and Food Chemistry, 2022, 70 (5): 1670–1678. doi: 10.1021/acs.jafc.1c07182
    [50]
    Urbaniak C, Cummins J, Brackstone M, et al. Microbiota of human breast tissue. Applied and Environmental Microbiology, 2014, 80 (10): 3007–3014. doi: 10.1128/AEM.00242-14
    [51]
    Thompson K J, Ingle J N, Tang X, et al. A comprehensive analysis of breast cancer microbiota and host gene expression. PLoS ONE, 2017, 12 (11): e0188873. doi: 10.1371/journal.pone.0188873
    [52]
    Ghoncheh M, Pournamdar Z, Salehiniya H. Incidence and mortality and epidemiology of breast cancer in the world. Asian Pacific Journal of Cancer Prevention, 2016, 17 (sup3): 43–46. doi: 10.7314/APJCP.2016.17.S3.43
    [53]
    Soto A M, Sonnenschein C. Environmental causes of cancer: endocrine disruptors as carcinogens. Nature Reviews Endocrinology, 2010, 6 (7): 363–370. doi: 10.1038/nrendo.2010.87
    [54]
    Goering P L, Aposhian H V, Mass M J, et al. The enigma of arsenic carcinogenesis: role of metabolism. Toxicological Sciences, 1999, 49 (1): 5–14. doi: 10.1093/toxsci/49.1.5
    [55]
    Sorahan T, Harrington J M. Lung cancer in Yorkshire chrome platers, 1972–97. Occupational & Environmental Medicine, 2000, 57 (6): 385–389. doi: 10.1136/oem.57.6.385
    [56]
    Lei Y X, Chen X M, Chen J K. Antisense translation elongation factor TEF_1δ reverses the carcinogenicity of cadmium chloride. Carcinogenesis, Teratogenesis and Mutagenesis, 2005, 17 (1): 1–4.
    [57]
    Liu X, Liu X, Wang H, et al. Phase separation drives decision making in cell division. Journal of Biological Chemistry, 2020, 295 (39): 13419–13431. doi: 10.1074/jbc.REV120.011746
    [58]
    Wang W, Yang F, Lin J, et al. Modeling of COVID-19 disease disparity in gastric organoids reveals the spatiotemporal dynamics of SARS-CoV-2 infectivity. Journal of Molecular Cell Biology, 2022, 14 (2): mjac007. doi: 10.1093/jmcb/mjac007
    [59]
    Poore G D, Kopylova E, Zhu Q, et al. Microbiome analyses of blood and tissues suggest cancer diagnostic approach. Nature, 2020, 579 (7800): 567–574. doi: 10.1038/s41586-020-2095-1
    [60]
    Gurbatri C R, Arpaia N, Danino T. Engineering bacteria as interactive cancer therapies. Science, 2022, 378 (6622): 858–864. doi: 10.1126/science.add9667
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