Voluntary exercise does not always suppress lung cancer progression

Leimbacher, Aurelia C.; Villiger, Philipp; Desboeufs, Nina; Aboouf, Mostafa A.; Armbruster, Julia; Ademi, Hyrije; Flüchter, Pascal; Ruetten, Maja; Gantenbein, Felix; Haider, Thomas; Gassmann, Max; Thiersch, Markus

doi:10.1016/j.isci.2023.107298

Cited by 3 publications

References 84 publications

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Multimodal prehabilitation enhances innate antitumor immunity via NK cell recruitment

Feng,

Gordon,

et al. 2024

Preprint

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BACKGROUNDWhile the clinical benefits of multimodal prehabilitation in cancer patients are well defined, the underlying immune modulations have not been studied. The objective of this study was to examine how prehabilitation can alter lung cancer immunity.METHODSNewly diagnosed lung cancer patients were referred to the prehabilitation clinic for preoperative personalized multimodal intervention (exercise training, nutritional optimization, and anxiety reduction) and blood samples were collected at baseline and surgery. Tumor samples were collected at surgery and compared to matched control samples from patients who did not receive prehabilitation. An animal model was used to study prehabilitation and tumor growth kinetics.RESULTSTwenty-eight lung cancer patients who underwent multimodal prehabilitation were included (McGill University Health Centre Research Ethics Board #2023-9005). After prehabilitation, patient-isolated peripheral blood mononuclear cells (PBMCs) showed significantly increased cytotoxicity against cancer cells (p< 0.0001) and significantly increased circulating natural killer (NK) cells in cohort (p= 0.0290) and paired analyses (p= 0.0312). Compared to matched controls, patients who received prehabilitation had significantly more intra-tumor NK cells (p= 0.0172).In vivo, we observed a significant increase in circulating NK cells (p= 0.0364) and slower tumor growth (p= 0.0396) with prehabilitation. When NK cells were depleted in prehabilitated mice, we observed a decrease in the protective effects of prehabilitation (p= 0.0314) and overall, we observed a significant correlation between circulating NK cells and reduced tumor volume (p= 0.0203, r = -0.5143).CONCLUSIONSMultimodal prehabilitation may play a role in antitumor immunity by increasing peripheral and tumour-infiltrating NK cells leading to a reduced cancer burden. Future studies on the protective effect of prehabilitation on postoperative immunity should be conducted.

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Multimodal prehabilitation enhances innate antitumor immunity via NK cell recruitment

Feng,

Gordon,

et al. 2024

Preprint

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Neospora caninum inhibits Lewis cancer and B16F10 melanoma lung metastasis development by activating the immune response in murine models

Qian,

Chen,

et al. 2024

Preprint

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Malignant tumors are prevalent with high mortality rates in humans, dogs, and cats. Some microorganisms have been shown to inhibit cancer progression. The objective of this study is to evaluate the inhibitory effects of Neospora caninum, a livestock parasite, on three different tumor models in C57BL/6 mice, including Lewis subcutaneous tumors, Lewis and B16F10 melanoma lung metastasis. The results showed that a sufficient amount of N. caninum tachyzoites can significantly inhibit the development of subcutaneous tumors and lung metastasis (P < 0.001), and induce more than 50% tumor cell death in Lewis subcutaneous tumors. N. caninum treatment can significantly increases the infiltration of macrophages, NK cells, and CD8+ T cells (P < 0.0001) in Lewis subcutaneous tumors detected by immunohistochemistry, and the percentage of these immunocytes in the spleen (P < 0.05) of mice bearing B16F10 melanoma metastasis detected by flow cytometry. And with these changes, the mRNA expression levels of IL-12, IFN-γ, IL-2, IL-10, TNF-α and PD-L1 in tumor microenvironment and IL-12, IFN-γ, IL-2 in spleen were also significantly increased (P < 0.05). Altogether, our results indicate that a sufficient amount N. caninum tachyzoites not only inhibits the growth of Lewis subcutaneous tumors, but inhibits the development of Lewis and B16F10 melanomas lung metastatic in mice by activating potent immune responses. N. caninum and its anti-tumor properties may be an effective anti-tumor tool.

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Exercise’s impact on lung cancer molecular mechanisms: a current overview

Mancini,

Orlandella,

Vitucci

et al. 2024

Front. Oncol.

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Lung cancer is the major cause of cancer-related deaths worldwide with an estimated 1.8 million deaths and 2.4 million new cases in 2022. Poor cardiorespiratory fitness, dyspnea and fatigue are the common features in lung cancer patients, partially limiting the exercise prescription. Exercise improves cardiorespiratory and muscular fitness and reduces the risk of some types of cancer, including lung cancer. Recently, the American Society of Clinical Oncology has encouraged preoperative exercise for lung cancer patients. Nonetheless, only limited data, mostly obtained from mouse models of lung cancer, are available on the molecular effects of exercise in lung cancer. Thus, the present minireview aims to shed light on the molecular mechanisms induced by different type of exercise in lung cancer. In particular, the role of the exercise in tumor microenvironment remodeling, angiogenesis, gene expression, apoptosis and intermediate metabolism will be examined.

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Voluntary exercise does not always suppress lung cancer progression

Cited by 3 publications

References 84 publications

Multimodal prehabilitation enhances innate antitumor immunity via NK cell recruitment

Multimodal prehabilitation enhances innate antitumor immunity via NK cell recruitment

Neospora caninum inhibits Lewis cancer and B16F10 melanoma lung metastasis development by activating the immune response in murine models

Exercise’s impact on lung cancer molecular mechanisms: a current overview

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