Pulmonary colonization of Candida albicans drives breast cancer lung metastasis via candidalysin

Z. Ma; L. Chen; Y. Fang; F. Gao; L. Liu; J. Wu; H. Chen; Y. Tian; Y. Zhang; X. Yang; Y. Wang; M. Ren; Y. Liu; L. Zhu; C. Chen; M. Guan; P. Tang; L. Wang; C. Li

doi:10.64898/2026.10.23.759946

AI summary · DOI: 10.64898/2026.10.23.759946 · bioRxiv: Cancer Biology

Pulmonary colonization of Candida albicans drives breast cancer lung metastasis via candidalysin

Z. Ma, L. Chen, Y. Fang, F. Gao, L. Liu, J. Wu, H. Chen, Y. Tian,

and 11 more authors

Y. Zhang, X. Yang, Y. Wang, M. Ren, Y. Liu, L. Zhu, C. Chen, M. Guan, P. Tang, L. Wang, C. Li

Original paper Published on 28 Oct. 2026 bioRxiv preprint License: CC BY-NC-ND 4.0 Also in: fr

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The essentials

The study reports that pulmonary Candida albicans promotes breast cancer lung metastasis through candidalysin-driven mast-cell activation and immune suppression.

Based on the abstract only: check the details in the original paper.

Question

The paper asks whether fungi colonizing distant organs influence tumor evolution, focusing on whether Candida albicans in the lungs affects breast cancer metastasis and through what mechanism.

Method

The authors examined fungal enrichment in breast cancer lung metastases and investigated the effects of candidalysin on pulmonary mast cells and the immune environment. They also compared clinical isolates and isogenic mutants with differing candidalysin secretion, and tested a combination regimen targeting fungal colonization, mast cells, and immunosuppression.

Findings

Result Candida albicans was selectively enriched in breast cancer lung metastases.
See the passage in the paper
Here, we identify selective enrichment of Candida albicans in breast cancer lung metastases.
Result Candidalysin activates pulmonary mast cells, which release mediators that expand immunosuppressive populations and suppress cytotoxic lymphocyte activity.
See the passage in the paper
Mechanistically, the fungal virulence factor candidalysin activates pulmonary mast cells, which release chemotactic mediators that expand immunosuppressive populations and suppress cytotoxic lymphocyte activity, remodeling the lung into a metastasis-permissive microenvironment.
Result Candidalysin secretion levels were associated with the metastasis-promoting potential of isolates and mutants.
See the passage in the paper
Analysis of clinical isolates and isogenic mutants further demonstrates that candidalysin secretion levels dictate metastasis-promoting potential.
Result A combination regimen targeting fungal colonization, mast cells, and the immunosuppressive environment curtailed metastatic progression.
See the passage in the paper
Informed by these findings, we developed a combination regimen that concurrently eliminates fungal colonization, stabilizes mast cells, and reverses the immunosuppressive microenvironment, thereby significantly curtailing metastatic progression.
Authors’ interpretation The authors frame pulmonary C. albicans colonization as a contributor to breast cancer lung metastasis and a potential therapeutic target.
See the passage in the paper
Collectively, our study establishes pulmonary C. albicans colonization as a driver of breast cancer lung metastasis and provides a mechanistic framework for targeting mycobiome-host interactions in metastatic disease.

Limitations

The supplied abstract does not report study details such as sample sizes, experimental models, or limitations, so the strength and scope of the findings cannot be assessed from this source alone.

Why it matters

The authors argue that fungi colonizing distant organs can shape metastatic progression, extending the study of cancer-associated mycobiomes beyond tumors themselves. They propose mycobiome-host interactions as a possible target in metastatic disease.

Written by AI from the paper. Passages are checked word for word against the text we analysed; the rest may contain errors.

AI-generated keywords: breast cancer metastasis Candida albicans candidalysin mast cells lung immune microenvironment

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Comprehensive Summary
Layman's Summary
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Original abstract

This bioRxiv preprint examines whether fungi in organs distant from a primary tumor can influence cancer progression. It focuses on whether *Candida albicans* in the lungs contributes to breast cancer metastasis there. The supplied material includes only the title and abstract, not the full paper. It therefore supports a summary of the authors’ reported findings but does not provide enough detail to fully assess the experiments or conclusions. The authors report that *C. albicans* was enriched in breast cancer lung metastases. They propose that candidalysin, a fungal virulence factor, activates lung mast cells. These cells then release chemotactic mediators that, according to the authors, expand immunosuppressive cell populations and reduce cytotoxic lymphocyte activity. Their account suggests that fungal colonization reshapes the lung environment, making it more permissive to metastatic growth. To investigate this proposed mechanism, the study reportedly examined fungal colonization and immune changes in the lungs. It also compared clinical *C. albicans* isolates with isogenic fungal mutants—strains that differ in a specific genetic feature—to assess candidalysin’s role. The abstract reports that candidalysin secretion levels were associated with the isolates’ ability to promote metastasis. This finding supports the authors’ claim that candidalysin contributes to the process. However, the abstract does not specify the number of isolates or mutants, how secretion was measured, or the size and design of the experiments. The authors also report developing a combination treatment intended to target three parts of the proposed process: fungal colonization, mast-cell activation, and the immunosuppressive environment. They state that the treatment significantly curtailed metastatic progression. The abstract does not provide the treatment components or doses, sample sizes, numerical effect estimates, or statistical results. It also does not clarify whether the regimen was tested in animals, patients, or both. The magnitude and robustness of the reported benefit therefore cannot be assessed from the supplied text. The paper’s central conclusion is that pulmonary *C. albicans* colonization may actively promote breast cancer lung metastasis, rather than merely accompany it. The authors propose candidalysin-mediated mast-cell activation as a link between the fungus and local immune suppression. Their findings motivate further investigation of microbial interactions with host immunity in metastatic organs and suggest that treatments targeting both fungal colonization and its downstream immune effects may warrant study. Several limitations are evident from the available information. Because only the abstract was supplied, the methods, controls, statistical analyses, patient cohort characteristics, and evidence for each step of the proposed mechanism cannot be independently assessed. The abstract also lacks key numerical results; no figures, effect estimates, or counts can be inferred. Finally, the work is described as a preprint, so its findings should be considered preliminary rather than established clinical evidence. The abstract does not show whether the proposed treatment is safe or effective in people, or whether the findings apply across breast cancer subtypes and patient populations.

Can a Lung Fungus Help Breast Cancer Spread?

A tumor does not grow in isolation. Cancer cells interact with immune cells and other features of the tissues around them—and, according to a new preprint, microbes in a distant organ may also shape whether cancer can take hold there. The study, titled “Pulmonary colonization of Candida albicans drives breast cancer lung metastasis via candidalysin,” examines whether the fungus Candida albicans can make the lungs more welcoming to breast cancer metastases.

The authors, Z. Ma, L. Chen, Y. Fang, F. Gao, L. Liu, J. Wu et al., report that C. albicans was enriched in lung metastases from breast cancer. They propose that the fungus does more than accompany metastatic disease: it may help create local conditions that favor cancer growth.

A Proposed Fungus–Immune–Cancer Connection

The proposed mechanism centers on candidalysin, a virulence factor produced by C. albicans. The authors suggest that candidalysin activates mast cells in the lung. Activated mast cells, in turn, release chemical signals that attract or expand immunosuppressive cell populations and weaken the activity of cytotoxic lymphocytes—immune cells that can attack cancer cells.

In this account, fungal colonization alters the lung’s immune environment. With fewer effective anti-cancer responses, metastatic cells may find it easier to survive and grow. The hypothesis links a fungal product to immune changes and, ultimately, to the progression of breast cancer in the lungs.

How the Study Examined the Hypothesis

According to the abstract, the researchers investigated fungal colonization and immune changes in the lungs. They also compared clinical C. albicans isolates with isogenic fungal mutants. Isogenic mutants are strains that differ in a specific genetic feature, allowing researchers to examine whether that feature affects an outcome.

The abstract reports that candidalysin secretion levels were associated with how strongly the isolates promoted metastasis. This association is consistent with the authors’ proposal that candidalysin helps drive the process. However, the summary does not say how many isolates or mutants were studied, how candidalysin secretion was measured, or how large the experiments were. It therefore does not allow readers to judge the strength of the evidence in detail.

A Combination Treatment

The authors also report developing a treatment intended to target three parts of their proposed pathway: fungal colonization, mast-cell activation, and the immunosuppressive environment. They state that the combination significantly curtailed metastatic progression.

That result is potentially interesting, but the abstract leaves important questions unanswered. It does not name the treatment components or doses, provide sample sizes or numerical effect estimates, or include statistical details. Nor does it clarify whether the regimen was tested in animals, patients, or both. Without that information, the size and robustness of the reported benefit cannot be assessed.

What the Findings May Mean

The paper’s central claim is that lung colonization by C. albicans may actively promote breast cancer metastasis, rather than simply appearing alongside it. If further research supports the proposed chain of events, it could broaden how scientists think about the metastatic environment: microbes in a target organ might influence the immune conditions cancer cells encounter.

The work also points toward a treatment strategy that addresses more than the fungus alone. Targeting colonization and downstream immune effects together could, in principle, disrupt several links in the proposed process. For now, however, this is a research direction—not evidence that such an approach is ready for clinical use.

Important Caveats

The available information is limited to the title and abstract, so the methods, controls, patient characteristics, and statistical analyses cannot be independently assessed. The abstract also provides no figures, counts, or effect estimates; none can be inferred from the summary. As a preprint, the work should be treated as preliminary rather than established clinical evidence.

Many questions remain. The supplied text does not establish whether the proposed treatment is safe or effective in people, or whether the findings apply across breast cancer subtypes and different patient populations. Further studies will be needed to test each step of the mechanism and determine how broadly the findings hold.

For now, the study offers a provocative hypothesis: a fungus in the lungs may influence local immunity in ways that favor metastatic growth. It adds to the case for investigating how microbes and the immune system interact in organs where cancer spreads, while leaving the clinical significance of this particular finding unresolved.

Created on 02 Nov. 2026

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Weekly letter Presented in "Biology and medicine this week" of 2 November 2026. Biology and medicine this week: Hidden partners, adjustable gates and overlooked disease

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Pulmonary colonization of Candida albicans drives breast cancer lung metastasis via candidalysin

The essentials

Question

Method

Findings

Limitations

Why it matters

Read further

Definitions

Can a Lung Fungus Help Breast Cancer Spread?

A Proposed Fungus–Immune–Cancer Connection

How the Study Examined the Hypothesis

A Combination Treatment

What the Findings May Mean

Important Caveats

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