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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)
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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).

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