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Peer-reviewedCC BYChemical biology & drug design

MSC C1: A Potential Hub Linking Stromal Plasticity, Immune Regulation, and Patient Survival in Lung Adenocarcinoma.

  • Houlei Wang1
  • Tianle Ma1
  • Chao Jia1
  • Chunhui Ma1
  1. 1Department of Orthopedics, Shanghai Geriatric Medical Center, Shanghai, China.
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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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Cite

BibTeXRIS
BibTeX
@article{wang2026potential,
  title = {{MSC C1: A Potential Hub Linking Stromal Plasticity, Immune Regulation, and Patient Survival in Lung Adenocarcinoma.}},
  author = {Houlei Wang and Tianle Ma and Chao Jia and Chunhui Ma},
  journal = {Chemical biology \& drug design},
  year = {2026},
  month = oct,
  doi = {10.1111/cbdd.70414},
  url = {https://europepmc.org/article/MED/42897747},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - MSC C1: A Potential Hub Linking Stromal Plasticity, Immune Regulation, and Patient Survival in Lung Adenocarcinoma.
AU  - Houlei Wang
AU  - Tianle Ma
AU  - Chao Jia
AU  - Chunhui Ma
PY  - 2026
DA  - 2026/10/01
JO  - Chemical biology & drug design
DO  - 10.1111/cbdd.70414
UR  - https://europepmc.org/article/MED/42897747
AB  - 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.
SN  - 1747-0277
SN  - 1747-0285
ER  -