ArticleCancer informatics2024
Cathepsin L in Lung Adenocarcinoma: Prognostic Significance and Immunotherapy Response Through a Multi Omics Perspective.
Article in Cancer informatics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Overexpression of ANAPC1 Affects the Cell Cycle Pathway to Promote the Progression of Lung Adenocarcinoma.Combinatorial chemistry & high throughput screening · 2026Article
- Cathepsin L as a dual-target to mitigate muscle wasting while enhancing anti-tumor efficacy of anti-PD-L1.Nature communications · 2025Article
- Elevated KIF2C Expression Drives Osteosarcoma Progression by Modulating the Wnt/β-Catenin Signaling Pathway and Contributing to an Immunosuppressive Tumor Microenvironment.Cancer medicine · 2025Article
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9 authors.
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Abstract
Objectives: Lung adenocarcinoma (LUAD), a predominant form of lung cancer, is characterized by a high rate of metastasis and recurrence, leading to a poor prognosis for LUAD patients. This study aimed to identify and rigorously validate a highly precise biomarker, Cathepsin L (CTSL), for the prognostic prediction of lung adenocarcinoma. Methods: We employed a multicenter and omics-based approach, analyzing RNA sequencing data and mutation information from public databases such as The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO). The DepMap portal with Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR/Cas9) technology was used to assess the functional impact of CTSL. Immunohistochemistry (IHC) was conducted on a local cohort to validate the prognostic significance of CTSL at the protein expression level. Results: Our findings revealed a significant correlation between elevated CTSL expression and advanced disease stage in LUAD patients. Kaplan-Meier survival analysis and Cox regression modeling revealed that high CTSL expression is associated with poor overall survival. The in vitro studies corroborated these findings, revealing notable suppression of tumor proliferation following CTSL knockout in cell lines, particularly in LUAD. Functional enrichment revealed that CTSL activated pathways associated with tumor progression, such as angiogenesis and Transforming growth factor beta (TGF-beta) signaling, and inhibited pathways such as apoptosis and DNA repair. Mutation analysis revealed distinct variations in the CTSL expression groups. Conclusion: This study highlights the crucial role of CTSL as a prognostic biomarker in LUAD. This combined multicenter and omics-based analysis provides comprehensive insights into the biological role of CTSL, supporting its potential as a target for therapeutic intervention and a marker for prognosis in patients with LUAD.
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