ArticleFrontiers in cell and developmental biology2025
Pan-cancer analysis of CHRDL1 expression and its mechanistic role in inhibiting EMT via the TGF-β pathway in lung adenocarcinoma.
Article in Frontiers in cell and developmental biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
- Pan-cancer analysis identifies KANSL2 as a cell-cycle-associated regulator of tumor progression and immunity in liver hepatocellular carcinoma.Clinical and experimental medicine · 2026Article
- Chorordin-like 1 inhibits pancreatic cancer cell migration and invasion: involvement of the BMP4/SMAD pathway.Frontiers in oncology · 2025Article
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Abstract
Background: The primary objective of this study is to conduct a pan-cancer analysis of CHRDL1 expression, to determine its correlation with patient survival rates, immune cell infiltration, and drug sensitivity. Additionally, the study aimed to further validate the mechanistic role of CHRDL1 in lung adenocarcinoma (LUAD), clarifying its contribution to tumorigenesis and evaluating its potential as a therapeutic target for LUAD. Methods: We employed bioinformatics strategies to analyze CHRDL1 expression using data from The Cancer Genome Atlas (TCGA) and the Genotype-Tissue Expression Project (GTEx). Survival analysis was executed with GEPIA2, while drug sensitivity to chemotherapeutic agents was evaluated via the CellMiner database. Mutational profiles were examined using cBioPortal, and the immune microenvironment was assessed through the TIMER database. To substantiate our findings, we conducted Results: CHRDL1 expression levels showed significant variation across different cancer types, with tumor tissues typically demonstrating lower expression compared to their normal counterparts. In certain cancers, elevated CHRDL1 expression was linked to poorer survival outcomes, whereas in LUAD, it was associated with improved survival. Furthermore, CHRDL1 expression correlated with the IC50 values of multiple chemotherapeutic drugs and played a role in modulating the immune microenvironment. We discovered that CHRDL1 inhibits the epithelial-mesenchymal transition (EMT) in LUAD through the TGF-β pathway. Conclusion: CHRDL1 exerts a complex influence on cancer development and progression, particularly in LUAD, by impacting tumor progression, immune regulation, chemosensitivity, and EMT regulation. This research offers valuable insights into the overarching mechanisms of cancer progression and aids in the discovery of innovative therapeutic strategies for LUAD treatment.
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