ArticleExperimental hematology & oncology2026
Single-cell profiling reveals FAM117A as a key regulator linking macrophage-epithelial crosstalk with the progression of lung adenocarcinoma.
Article in Experimental hematology & oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- The evolving role of OMICS in gastrointestinal tumor biology and clinical practice.Molecular cancer · 2026Review
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9 authors.
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Abstract
The tumor microenvironment (TME) has a profound influence on the progression of lung adenocarcinoma (LUAD) and its response to therapy. We identified a tumor-promoting communication network based on single-cell RNA sequencing. This shows an SPP1 + macrophage and basal epithelial cell communication module (CIM) that is enriched in invasive portions of tumors, and spatially associated with decreased cytotoxic T cell activity and poor prognosis. Transcriptomic modeling identified FAM117A as a major suppressor of the CIM network. FAM117A is a DYRK1A-interacting cell-cycle regulator. Loss of FAM117A resulted in longer G1/S transition time, increased cell proliferation, and an enhanced macrophage-epithelial feedback loop. Immunohistochemical studies showed decreased FAM117A expression in LUAD tissues, which correlated with SPP1 + macrophage density and poor outcome. Treatment with FAM117A or pharmacological inhibition of CDK4/6 reduced the in vitro and in vivo tumor growth. Thus, FAM117A links intrinsic cell cycle regulation with the extrinsic immune microenvironment, providing a rationale for combined therapies that address macrophage-tumor and cell cycle regulatory events in LUAD.
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