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CALD1 promotes the expression of PD-L1 in bladder cancer via the JAK/STAT signaling pathway
Cheng Li1,2, Fuhan Yang1,2, Ruiliang Wang1,2
1Department of Urology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China.
Background:
Bladder cancer (BC) is a common malignant neoplasm with a high rate of recurrence and progression, despite optimal treatment. There is a pressing need to identify new effective biomarkers for the targeted treatment of BC.
Methods:
The key gene CALD1 was screened via weighed gene co-expression network analysis (WGCNA) from encoding protein genes of BC. Clinical and prognostic significance was explored in The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. Cell Counting Kit-8 (CCK-8), flow cytometry, transwell chamber experiment and nude mouse xenograft assay were performed to test cell growth, apoptosis, migration, invasion and tumorigenesis capacities. Immune correlation was analyzed in The Tumor Immune Estimation Resource (TIMER) database. Relevant signaling pathways were explored using gene set enrichment analysis (GSEA).
Results:
Increased expression of CALD1 was significantly correlated with histological grade, clinical stage, T stage, and lymphatic metastasis. Kaplan-Meier survival curves showed that high CALD1 expression was associated with poor overall survival (OS) and disease-free survival (DFS) in TCGA database, and with poor OS in the four GEO databases. CALD1 promotes growth, migration, invasion, and cell cycle of tumor cell, and inhibits tumor cell apoptosis in vitro and in vivo. CADL1 expression was positively correlated with increased CD274 levels (r=0.357, P=9.71e-14). JAK/STAT signaling pathway was significantly enriched in the high CALD1 expression group. CALD1-mediated PD-L1 overexpression (OE) was via the activation of the JAK/STAT signaling pathway; this effect was blocked by the specific JAK inhibitor Ruxolitinib.
Conclusions:
CALD1 is a potential molecular marker associated with prognosis. It promotes the malignant progression of BC and upregulates the PD-L1 expression via the JAK/STAT signaling pathway.
Insights
The gene CALD1 is a potential biomarker for bladder cancer (BC). High CALD1 expression correlates with poor prognosis and promotes BC progression by upregulating PD-L1 via the JAK/STAT pathway.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Bladder cancer (BC) is a prevalent malignancy with high recurrence rates.
- Effective biomarkers are needed for targeted BC treatment.
- Identifying novel prognostic markers is crucial for improving patient outcomes.
Purpose of the Study:
- To investigate the role of the gene CALD1 as a potential biomarker in bladder cancer.
- To explore the correlation between CALD1 expression and clinical-pathological features and prognosis of BC.
- To elucidate the underlying molecular mechanisms of CALD1 in BC progression.
Main Methods:
- Weighted gene co-expression network analysis (WGCNA) for key gene screening.
- Analysis of clinical and prognostic data from TCGA and GEO databases.
- In vitro and in vivo assays to assess cell growth, apoptosis, migration, and invasion.
- Immune correlation analysis using TIMER database and pathway analysis via GSEA.
Main Results:
- CALD1 expression positively correlated with tumor grade, stage, and metastasis.
- High CALD1 expression was associated with poorer overall survival and disease-free survival.
- CALD1 promoted tumor cell proliferation, migration, invasion, and cell cycle, while inhibiting apoptosis.
- CALD1 upregulated PD-L1 expression via JAK/STAT pathway activation.
Conclusions:
- CALD1 serves as a potential prognostic molecular marker for bladder cancer.
- CALD1 facilitates malignant progression of BC.
- CALD1 upregulates PD-L1 expression through the JAK/STAT signaling pathway.
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