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NPM3 as a novel oncogenic factor and poor prognostic marker contributes to cell proliferation and migration in lung
Shan Wei1,2, Jing Xing2,3, Kaining Lu4
1Department of Respiratory and Critical Care Medicine, The Fourth Affiliated Hospital, School of Medicine, Zhejiang University, Yiwu, 322000, Zhejiang, People's Republic of China.
Background:
Lung cancer is the leading cause of cancer-related deaths worldwide, and despite recent advances in targeted therapies and immunotherapies, the clinical benefit remains limited. Therefore, there is an urgent need to further investigate the molecular mechanisms underlying lung cancer. The aim of this study was to investigate the expression and function of NPM3 in the tumor microenvironment of lung adenocarcinoma (LUAD).
Methods:
We utilized bioinformatics tools and databases, including UALCAN, GEPIA2, HPA, and Sangerbox, to analyze NPM3 expression in LUAD samples and its association with prognosis and mutational landscape. NPM3 expression in various cell types was assessed at the single cell level using the TISCH database. We also used algorithms such as TIMER and EPIC to explore the crosstalk between NPM3 expression and immune features. KEGG enrichment analysis was performed to identify potential signaling pathways of NPM3. Finally, we employed siRNA knockdown strategy to investigate the effect of NPM3 on LUAD cell proliferation and migration in vitro.
Results:
NPM3 was significantly upregulated in LUAD tissues and was strongly associated with poor prognosis and TP53 gene mutations. Single-cell sequencing analysis revealed that NPM3 was expressed in immune cells (dendritic cells and monocytes/macrophages) in the tumor microenvironment. Moreover, NPM3 expression was negatively associated with immune B cell and CD4 T cell infiltration, as well as with several immune-related genes (including CCL22, CXCR2, CX3CR1, CCR6, HLA-DOA, HLA-DQA2). KEGG enrichment analysis indicated that NPM3 expression was associated with cell cycle, CAMs, and NSCLC pathway genes. Finally, in vitro experiments showed that NPM3 knockdown inhibited LUAD cell proliferation and migration in NCI-H1299 and SPC-A1 cells, and suppressed the expression of CCNA2 and MAD2L1.
Conclusion:
Elevated NPM3 expression predicts poor clinical outcome and an immunosuppressive microenvironment in LUAD tissues. NPM3 promotes LUAD progression by promoting cell proliferation and migration, and targeting NPM3 may represent a novel therapeutic strategy for LUAD.
Insights
Nucleophosmin 3 (NPM3) is upregulated in lung adenocarcinoma (LUAD), correlating with poor prognosis and an immunosuppressive tumor microenvironment. Targeting NPM3 may offer a new therapeutic strategy for LUAD patients.
Area of Science:
- Oncology
- Molecular Biology
- Immunology
Background:
- Lung cancer remains a leading cause of cancer mortality globally.
- Current therapies show limited clinical benefit, necessitating deeper understanding of lung cancer molecular mechanisms.
- Investigating NPM3 in the lung adenocarcinoma (LUAD) tumor microenvironment is crucial.
Purpose of the Study:
- To investigate the expression and function of NPM3 in the LUAD tumor microenvironment.
- To analyze the association of NPM3 with prognosis, immune infiltration, and signaling pathways in LUAD.
- To evaluate the impact of NPM3 on LUAD cell behavior in vitro.
Main Methods:
- Bioinformatics analysis using UALCAN, GEPIA2, HPA, and Sangerbox for NPM3 expression and prognosis.
- Single-cell analysis (TISCH) to assess NPM3 expression in tumor-infiltrating cells.
- Immune infiltration analysis using TIMER and EPIC algorithms.
- KEGG pathway enrichment analysis.
- In vitro siRNA knockdown experiments in LUAD cell lines.
Main Results:
- NPM3 is significantly upregulated in LUAD and linked to poor prognosis and TP53 mutations.
- NPM3 expression in immune cells (dendritic cells, macrophages) negatively correlates with B cell and CD4 T cell infiltration.
- NPM3 is associated with cell cycle, CAMs, and NSCLC pathways.
- NPM3 knockdown inhibits LUAD cell proliferation and migration, suppressing CCNA2 and MAD2L1.
Conclusions:
- High NPM3 expression indicates poor clinical outcome and an immunosuppressive LUAD microenvironment.
- NPM3 promotes LUAD progression via enhanced cell proliferation and migration.
- Targeting NPM3 presents a potential novel therapeutic strategy for LUAD.
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