Respiratory viral infection promotes the awakening and outgrowth of dormant metastatic breast cancer cells in lungs [RNA-seq]
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ABSTRACT:
PROVIDER: PRJNA1188584 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR31414736_1.fastq.gz | Fastqsanger.gz | |||
| SRR31414736_2.fastq.gz | Fastqsanger.gz | |||
| SRR31414737_1.fastq.gz | Fastqsanger.gz | |||
| SRR31414737_2.fastq.gz | Fastqsanger.gz | |||
| SRR31414738_1.fastq.gz | Fastqsanger.gz |
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Project description:Respiratory viral infection promotes the awakening and outgrowth of dormant metastatic breast cancer cells in lungs
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Project description:Breast cancer is the second most common cancer globally. Most deaths from breast cancer are due to metastatic disease which often follows long periods of clinical dormancy. Understanding the mechanisms that disrupt the quiescence of dormant disseminated cancer cells (DCC) is crucial for addressing metastatic progression. Infection with respiratory viruses (e.g. influenza or SARS-CoV-2) is common and triggers an inflammatory response locally and systemically. Here we show that influenza virus infection leads to loss of the pro-dormancy mesenchymal phenotype in breast DCC in the lung, causing DCC proliferation within days of infection, and a greater than 100-fold expansion of carcinoma cells into metastatic lesions within two weeks. Such DCC phenotypic change and expansion is interleukin-6 (IL-6)-dependent. We further show that CD4 T cells are required for the maintenance of pulmonary metastatic burden post-influenza virus infection, in part through attenuation of CD8 cell responses in the lungs. Single-cell RNA-seq analyses reveal DCC-dependent impairment of T-cell activation in the lungs of infected mice. SARS-CoV-2 infected mice also showed increased breast DCC expansion in lungs post-infection. Expanding our findings to human observational data, we observed that cancer survivors contracting a SARS-CoV-2 infection have substantially increased risks of lung metastatic progression and cancer related death compared to cancer survivors who did not. These discoveries underscore the significant impact of respiratory viral infections on the resurgence of metastatic cancer, offering novel insights into the interconnection between infectious diseases and cancer metastasis.
2025-05-27 | GSE264175 | GEO
Project description:Breast cancer is the second most common cancer globally, with most deaths caused by metastatic disease, often following long periods of clinical dormancy1. Understanding the mechanisms that disrupt the quiescence of dormant disseminated cancer cells (DCC) is crucial for addressing metastatic progression. Respiratory viruses infections such as influenza or SARS-CoV-2, trigger both local and systemic inflammation2,3. Here we demonstrate that influenza virus and SARS-CoV-2 infections lead to loss of the pro-dormancy phenotype in breast DCC in the lung, causing DCC proliferation within days of infection, and a massive expansion of carcinoma cells into metastatic lesions within two weeks. This phenotypic transition and expansion are interleukin-6 (IL-6)-dependent. We show that CD4+ T cells sustain pulmonary metastatic burden post-influenza infection by suppressing CD8+ T cell responses. Additionally, DCCs impair lung T-cell activation and tumor cell killing in infected mice. Critically, these experimental findings align with human observational data. Analyses of cancer survivors from the UK Biobank and Flatiron Health databases reveal that SARS-CoV-2 infection substantially increases the risk of lung metastasis and cancer-related mortality compared to uninfected cancer survivors. Notably, the heightened risk is most pronounced in the months following infection, paralleling experimental observations of accelerated DCC proliferation and metastatic progression shortly after viral infection. These discoveries underscore the significant impact of respiratory viral infections on metastatic cancer resurgence, offering novel insights into the interconnection between infectious diseases and cancer metastasis.
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Project description:The awakening of dormant disseminated cancer cells appears to be responsible for the clinical relapses of patients whose primary tumors have been successfully cured months and even years earlier. In the present study, we demonstrate that dormant breast cancer cells lodged in the lungs reside in a highly mesenchymal, non-proliferative phenotypic state. The awakening of these cells is not triggered by a cancer cell-autonomous process. Instead, lung inflammation induced by the chemotherapeutic agent bleomycin effectively awakens dormant cancer cells, providing useful models for studying metastatic awakening. Mechanistically, the awakened cells shift from a highly mesenchymal to a quasi-mesenchymal phenotypic state in which they acquire tumorigenicity and proliferative ability. Once awakened, these cells can stably reside in this quasi-mesenchymal state and maintain their tumor-initiating ability, doing so without ongoing heterotypic signaling from the lung microenvironment. EGFR ligands released by the cells of the injured tissue microenvironment, including notably M2 type macrophages, promote dormant cancer cells to move toward this quasi-mesenchymal state, a transition that is critical for the awakening process. An understanding of the mechanisms of metastatic awakening may lead in the future to treatment strategies designed to prevent such awakening and resulting metastatic relapse.
2025-08-19 | GSE280817 | GEO
Project description:The awakening of dormant disseminated cancer cells is responsible for the clinical relapses of patients whose primary tumors have been cured months and even years earlier. In the present study, we demonstrate that dormant breast cancer cells lodged in the lungs reside in a highly mesenchymal, non-proliferative phenotypic state. The awakening of these cells does not occur because of a cancer cell-autonomous process. Instead, inflammation and wound-healing of the surrounding tissue microenvironment causes them to shift from a highly mesenchymal to a quasi-mesenchymal phenotypic state in which they acquire stemness and proliferative ability. Once awakened, these cells can stably reside in this quasi-mesenchymal state and maintain their stemness, doing so without ongoing heterotypic signaling from the lung microenvironment. EGFR ligands released by the cells of the injured tissue microenvironment, including notably M2 type macrophages, promote dormant cancer cells to move toward this quasi-mesenchymal state, a transition that is essential for the awakening process. An understanding of the mechanisms of metastatic awakening may lead in the future to treatment strategies designed to prevent such awakening and resulting metastatic relapse.
2025-08-19 | GSE289726 | GEO
Project description:The awakening of dormant disseminated cancer cells is responsible for the clinical relapses of patients whose primary tumors have been cured months and even years earlier. In the present study, we demonstrate that dormant breast cancer cells lodged in the lungs reside in a highly mesenchymal, non-proliferative phenotypic state. The awakening of these cells does not occur because of a cancer cell-autonomous process. Instead, inflammation and wound-healing of the surrounding tissue microenvironment causes them to shift from a highly mesenchymal to a quasi-mesenchymal phenotypic state in which they acquire stemness and proliferative ability. Once awakened, these cells can stably reside in this quasi-mesenchymal state and maintain their stemness, doing so without ongoing heterotypic signaling from the lung microenvironment. EGFR ligands released by the cells of the injured tissue microenvironment, including notably M2 type macrophages, promote dormant cancer cells to move toward this quasi-mesenchymal state, a transition that is essential for the awakening process. An understanding of the mechanisms of metastatic awakening may lead in the future to treatment strategies designed to prevent such awakening and resulting metastatic relapse.
2025-08-19 | GSE266952 | GEO
Project description:The awakening of dormant disseminated cancer cells is responsible for the clinical relapses of patients whose primary tumors have been cured months and even years earlier. In the present study, we demonstrate that dormant breast cancer cells lodged in the lungs reside in a highly mesenchymal, non-proliferative phenotypic state. The awakening of these cells does not occur because of a cancer cell-autonomous process. Instead, inflammation and wound-healing of the surrounding tissue microenvironment causes them to shift from a highly mesenchymal to a quasi-mesenchymal phenotypic state in which they acquire stemness and proliferative ability. Once awakened, these cells can stably reside in this quasi-mesenchymal state and maintain their stemness, doing so without ongoing heterotypic signaling from the lung microenvironment. EGFR ligands released by the cells of the injured tissue microenvironment, including notably M2 type macrophages, promote dormant cancer cells to move toward this quasi-mesenchymal state, a transition that is essential for the awakening process. An understanding of the mechanisms of metastatic awakening may lead in the future to treatment strategies designed to prevent such awakening and resulting metastatic relapse.
2025-08-19 | GSE266953 | GEO
Project description:Awakening and Eliminating Dormant Cancer Cells: A Foundation for Resistance Removal and Recurrence-Free Recovery
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Project description:Bacillus subtilis forms dormant spores upon nutrient depletion. Under favorable environmental conditions, the spore breaks its dormancy and resumes growth in a process called spore germination and outgrowth. To elucidate the physiological processes that occur during the transition of the dormant spore to an actively growing vegetative cell, we studied this process in a time-dependent manner by a combination of microscopy, analysis of extracellular metabolites and a genome-wide analysis of transcription. The results indicate the presence of abundant levels of late sporulation transcripts in dormant spores. In addition, results suggest the existence of a complex and well-regulated spore outgrowth program, involving the temporal expression of at least 30 % of the B. subtilis genome. Keywords: time course, spore outgrowth
2007-03-27 | GSE6865 | GEO
Project description:The goal of this study is to compare the trancriptome of proliferative THEP3 cells to their dormant counterpart DHEP3 and an awaken version through DDR1 receptor depletion (shRNA control verus shRNA DDR1) to identify target genes involved in the dormancy state and the awakening process from where metatsiss will arise.
2021-10-20 | GSE182890 | GEO