ArticleChemical biology & drug design2026
MSC C1: A Potential Hub Linking Stromal Plasticity, Immune Regulation, and Patient Survival in Lung Adenocarcinoma.
Article in Chemical biology & drug design, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Bone metastasis of lung adenocarcinoma (LUAD) directly leads to poor prognosis. This study aimed to dissect the stromal landscape of LUAD with bone metastases. Unsupervised clustering of scRNA-seq data from LUAD patients with bone metastasis identifies stromal subsets. Pseudotime analysis combined with CytoTRACE stemness scoring reconstructs mesenchymal stromal cell (MSC) differentiation trajectories, while CellChat characterizes cell-cell communication networks among MSC subpopulations. Differentially expressed genes (DEGs) specific to functionally distinct MSC subsets are subjected to LASSO-Cox regression for construction of a prognostic RiskScore model, which is validated in independent bulk RNA-seq cohorts regarding overall survival, immune cell infiltration, and drug sensitivity. A distinct high-stemness MSC C1 subpopulation is localized at the bifurcation point of two divergent differentiation trajectories toward a matrix-remodeling fate and a secretory, immunomodulatory phenotype. The RiskScore model stratifies patients into low- and high-risk groups with divergent overall-survival outcomes. Reduced infiltration of cytotoxic lymphocytes is observed in high-risk patients, and higher drug sensitivity within the high-risk subgroup. In vitro assays verify that LDHA knockdown impairs proliferation and migration in A549 cells. This study provides a rationale for targeting stroma-derived genes in risk-adapted therapy.
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