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Peer-reviewedCC BYChemical biology & drug design

Single-Cell Dissection of Inflammatory Suppression and Stemness Plasticity Reveals STMN1-Associated Malignant Epithelial Cells in Severe Lung Cancer.

  • Yanmei Chen1
  • Sisi Chen2
  • Biao Cheng3
  • Yuzhu Tang3
  • Yiyan Huang4
  • Miao Chen5
5 affiliations
  1. 1Department of Endocrinology, The Affiliated Yongchuan Hospital of Chongqing Medical University, Chongqing, China.
  2. 2Chongqing Medical and Pharmaceutical College, Chongqing, China.
  3. 3Department of Oncology, Xinqiao Hospital, Army Medical University (Third Military Medical University), Chongqing, China.
  4. 4Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, China.
  5. 5Institute of Health Sciences, China Medical University, Shenyang, Liaoning, China.
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Abstract

The disease course in patients with advanced lung cancer with malignant serous effusions (ALC-MSE) is complex, and treatment outcomes are difficult to predict; systematic studies on the tumor stem cell-like characteristics and regulatory mechanisms of this condition are still lacking. Based on single-cell transcriptomic data and the TCGA-LUAD cohort, this study systematically analyzed the functional characteristics and key regulatory networks of malignant epithelial cells in severe lung cancer. Key findings include: epithelial cells in severe lung cancer exhibit significantly attenuated inflammation- and immunity-related signaling pathways (including NF-κB, TNF, and JAK-STAT signaling pathways), enhanced stem cell-like properties, and metabolic reprogramming; we identified a highly stem-like malignant epithelial cell subpopulation, represented by Cluster 3, which is enriched in stem-like pathways such as Notch, Hippo, TGF-β, and FoxO, and is accompanied by enhanced mitochondrial metabolism and stress adaptability; STMN1 is a key molecule regulating this stem-like state, showing a significant positive correlation with stemness scores and mRNAi; cells with high STMN1 expression gain a survival advantage and may maintain their stemness by attenuating CAF/ECM signaling with other cells (COL1A1-CD44), inhibiting complement activation and antigen presentation signaling (such as C3, ANXA1, and MHC-II-related molecules), and enhancing stemness niche signaling (MIF-CD74/CD44). Furthermore, NELFE, MYBL2, FOXN3, POLR2A, and RAD21 were identified as potential upstream regulators of STMN1. In vitro experiments confirmed that, following induction of stem cell-like properties, STMN1 was significantly overexpressed in lung adenocarcinoma cells, accompanied by upregulation of related stem cell markers (SOX2, NANOG, OCT4, and CD44). In summary, this study reveals a significantly enhanced stemness state in malignant epithelial cells in advanced lung cancer, accompanied by suppressed inflammatory signaling and enhanced metabolic adaptation, and identifies STMN1 as a key molecule driving stemness maintenance and disease progression.

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Cite

BibTeXRIS
BibTeX
@article{chen2026singlecell,
  title = {{Single-Cell Dissection of Inflammatory Suppression and Stemness Plasticity Reveals STMN1-Associated Malignant Epithelial Cells in Severe Lung Cancer.}},
  author = {Yanmei Chen and Sisi Chen and Biao Cheng and Yuzhu Tang and Yiyan Huang and Miao Chen},
  journal = {Chemical biology \& drug design},
  year = {2026},
  month = oct,
  doi = {10.1111/cbdd.70420},
  url = {https://europepmc.org/article/MED/42904604},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Single-Cell Dissection of Inflammatory Suppression and Stemness Plasticity Reveals STMN1-Associated Malignant Epithelial Cells in Severe Lung Cancer.
AU  - Yanmei Chen
AU  - Sisi Chen
AU  - Biao Cheng
AU  - Yuzhu Tang
AU  - Yiyan Huang
AU  - Miao Chen
PY  - 2026
DA  - 2026/10/01
JO  - Chemical biology & drug design
DO  - 10.1111/cbdd.70420
UR  - https://europepmc.org/article/MED/42904604
AB  - The disease course in patients with advanced lung cancer with malignant serous effusions (ALC-MSE) is complex, and treatment outcomes are difficult to predict; systematic studies on the tumor stem cell-like characteristics and regulatory mechanisms of this condition are still lacking. Based on single-cell transcriptomic data and the TCGA-LUAD cohort, this study systematically analyzed the functional characteristics and key regulatory networks of malignant epithelial cells in severe lung cancer. Key findings include: epithelial cells in severe lung cancer exhibit significantly attenuated inflammation- and immunity-related signaling pathways (including NF-κB, TNF, and JAK-STAT signaling pathways), enhanced stem cell-like properties, and metabolic reprogramming; we identified a highly stem-like malignant epithelial cell subpopulation, represented by Cluster 3, which is enriched in stem-like pathways such as Notch, Hippo, TGF-β, and FoxO, and is accompanied by enhanced mitochondrial metabolism and stress adaptability; STMN1 is a key molecule regulating this stem-like state, showing a significant positive correlation with stemness scores and mRNAi; cells with high STMN1 expression gain a survival advantage and may maintain their stemness by attenuating CAF/ECM signaling with other cells (COL1A1-CD44), inhibiting complement activation and antigen presentation signaling (such as C3, ANXA1, and MHC-II-related molecules), and enhancing stemness niche signaling (MIF-CD74/CD44). Furthermore, NELFE, MYBL2, FOXN3, POLR2A, and RAD21 were identified as potential upstream regulators of STMN1. In vitro experiments confirmed that, following induction of stem cell-like properties, STMN1 was significantly overexpressed in lung adenocarcinoma cells, accompanied by upregulation of related stem cell markers (SOX2, NANOG, OCT4, and CD44). In summary, this study reveals a significantly enhanced stemness state in malignant epithelial cells in advanced lung cancer, accompanied by suppressed inflammatory signaling and enhanced metabolic adaptation, and identifies STMN1 as a key molecule driving stemness maintenance and disease progression.
SN  - 1747-0277
SN  - 1747-0285
ER  -