![]() ![]() ![]() ![]() Collectively, our findings demonstrate the critical pathological role of activin A-producing AMs in tumorigenesis, and provides means to clearly distinguish them from their healthy counterparts.Ĭancerous tissues comprise a wide variety of cells in addition to tumor cells, such as immune cells, fibroblasts 1, endothelial cells 2, and neural cells 3, which constitute unique microenvironments specific to the cancer cell type. Moreover, postnatal deletion of INHBA/activin A could limit tumor growth in experimental models. Single-cell RNA sequence analysis identifies a characteristic subset of AMs specifically induced in the tumor environment that are abundant in INHBA, and distinct from INHBA-expressing AMs in normal lungs. Accordingly, follistatin, an antagonist of activin A is able to inhibit lung cancer cell proliferation. Inhibin beta A (INHBA) expression is upregulated in AMs under tumor-bearing conditions, leading to the secretion of activin A, a homodimer of INHBA. Here we show, using an orthotopic murine lung cancer model and human carcinoma samples, that AMs support cancer cell proliferation and thus contribute to unfavourable outcome. They are abundant in lung cancer tissues, but their pathophysiological significance remains unknown. Alveolar macrophages (AMs) are crucial for maintaining normal lung function. ![]()
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