High Level of Component C1q Binding Protein (C1QBP) is Associated With Poor Prognosis and Dysfunction of Mast Cells in Lung Adenocarcinoma.
- 1Department of Respiratory and Critical Care Medicine, Second Affiliated Hospital of Xi'an JiaoTong University, Xi'an City, Shaanxi Province, China.
- 2Department of Respiratory and Critical Care Medicine, Bainiaohu Branch of People's Hospital of Xinjiang Uygur Autonomous Region, Urumqi City, Xinjiang Uigur Autonomous Region, China.
Abstract
Background
Component C1q binding protein (C1QBP) is known as an important regulator of mitochondrial plasticity and is involved in antitumor immune response in cancers. Nevertheless, its role in lung adenocarcinoma (LUAD) still remains largely unknown.Methods
C1QBP expression in LUAD and adjacent normal samples was compared by Wilcoxon test, and the corresponding receiver operating characteristic (ROC) curve was used to estimate its diagnostic value. Associations between C1QBP expression levels and different clinical traits were analyzed by chi-square test; K-M curves were applied for analyzing survival differences, and univariate and multivariate Cox analysis were employed to construct the C1QBP-related nomogram model. Furthermore, GSEA and immune analysis were performed to explore the mechanism. Finally, rhC1QBP was applied to cultured mast cells in vivo to investigate its regulatory effect on mast cell dysfunction, and sh-C1QBP was injected into LUAD xenograft mice to explore the effect of C1QBP knockdown on tumor growth in vivo.Results
The C1QBP expression level, with a preferable diagnosis effect, was significantly different between LUAD and normal samples, and was notably interrelated with gender, TNM stage, and Fustat in LUAD patients. LUAD patients with high C1QBP levels displayed lower survival rates. Our nomogram based on C1QBP expression and T stage displayed decent prediction capability. There was a significant difference in C1QBP expression in plasma cells, regulatory T cells (Tregs), activated CD4 memory T cells, resting mast cells, and eosinophils between LUAD patients and the controls. Upregulation of C1QBP with rhC1QBP treatment promoted mast cell ferroptosis through interacting with the Cullin3 protein. While Fer-1, a ferroptosis inhibitor, counteracted rhC1QBP induced ferroptosis in mast cells. Knockdown of C1QBP inhibited tumor growth in xenograft mice.Conclusion
C1QBP may be a promising potential prognostic biomarker in LUAD and a potential therapeutic target by affecting the immune microenvironment of LUAD patients.
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BibTeX
@article{li2026high,
title = {{High Level of Component C1q Binding Protein (C1QBP) is Associated With Poor Prognosis and Dysfunction of Mast Cells in Lung Adenocarcinoma.}},
author = {Wei Li and Guangnan Huang and Lizhong Zeng and Wenhui Dang and Ting Jiao and Yonghong Zhang and Mengying Zhang and Shuru Zhou and Liping Chen and Shuanying Yang},
journal = {Cancer medicine},
year = {2026},
month = oct,
doi = {10.1002/cam4.72394},
url = {https://europepmc.org/article/MED/42952304},
note = {CC BY-NC-ND},
}
RIS
TY - JOUR
TI - High Level of Component C1q Binding Protein (C1QBP) is Associated With Poor Prognosis and Dysfunction of Mast Cells in Lung Adenocarcinoma.
AU - Wei Li
AU - Guangnan Huang
AU - Lizhong Zeng
AU - Wenhui Dang
AU - Ting Jiao
AU - Yonghong Zhang
AU - Mengying Zhang
AU - Shuru Zhou
AU - Liping Chen
AU - Shuanying Yang
PY - 2026
DA - 2026/10/29
JO - Cancer medicine
DO - 10.1002/cam4.72394
UR - https://europepmc.org/article/MED/42952304
AB - Background Component C1q binding protein (C1QBP) is known as an important regulator of mitochondrial plasticity and is involved in antitumor immune response in cancers. Nevertheless, its role in lung adenocarcinoma (LUAD) still remains largely unknown.Methods C1QBP expression in LUAD and adjacent normal samples was compared by Wilcoxon test, and the corresponding receiver operating characteristic (ROC) curve was used to estimate its diagnostic value. Associations between C1QBP expression levels and different clinical traits were analyzed by chi-square test; K-M curves were applied for analyzing survival differences, and univariate and multivariate Cox analysis were employed to construct the C1QBP-related nomogram model. Furthermore, GSEA and immune analysis were performed to explore the mechanism. Finally, rhC1QBP was applied to cultured mast cells in vivo to investigate its regulatory effect on mast cell dysfunction, and sh-C1QBP was injected into LUAD xenograft mice to explore the effect of C1QBP knockdown on tumor growth in vivo.Results The C1QBP expression level, with a preferable diagnosis effect, was significantly different between LUAD and normal samples, and was notably interrelated with gender, TNM stage, and Fustat in LUAD patients. LUAD patients with high C1QBP levels displayed lower survival rates. Our nomogram based on C1QBP expression and T stage displayed decent prediction capability. There was a significant difference in C1QBP expression in plasma cells, regulatory T cells (Tregs), activated CD4 memory T cells, resting mast cells, and eosinophils between LUAD patients and the controls. Upregulation of C1QBP with rhC1QBP treatment promoted mast cell ferroptosis through interacting with the Cullin3 protein. While Fer-1, a ferroptosis inhibitor, counteracted rhC1QBP induced ferroptosis in mast cells. Knockdown of C1QBP inhibited tumor growth in xenograft mice.Conclusion C1QBP may be a promising potential prognostic biomarker in LUAD and a potential therapeutic target by affecting the immune microenvironment of LUAD patients.
SN - 2045-7634
ER -