CNGB3 promotes proliferation migration and metastasis in gastric cancer cells

Abstract AIM: To investigate CNGB3 as a prognostic biomarker and functional driver of gastric cancer progression. MATERIALS AND METHODS: We used multi-omics approaches to comprehensively evaluate CNGB3's role in gastric cancer. Transcriptomic and clinical data were retrieved from the TCGA, GTEx, and GEO (GSE84437) databases. Analyzed methods included differential expression analysis between tumor and normal tissues, functional enrichment analysis (GO, KEGG, GSEA), immune infiltration analysis using the ssGSEA algorithm, and Kaplan-Meier survival analysis with Cox regression modeling. RESULTS: CNGB3 expression levels in gastric cancer tissues were significantly elevated compared to normal tissues, and even higher in metastatic gastric cancer (p < 0.05). Differential expression analysis identified 2,059 differentially expressed genes (|log2FC| > 1), from which 20 hub genes were identified through PPI network construction. Immune infiltration analysis showed substantial differences in immune cell enrichment between high and low CNGB3 expression groups (p < 0.001), including elevated activated NK cells and CD8+ T cells, suggesting CNGB3 may influence gastric cancer immune evasion by modulating the tumor microenvironment. Kaplan-Meier survival analysis indicated that overall survival, disease-specific survival, and progression-free survival rates were markedly reduced in the high CNGB3 expression group compared to the low expression group (p < 0.05). These findings reveal for the first time CNGB3's role as a prognostic biomarker across cancer types. The association between CNGB3 expression and immune cell infiltration suggests its involvement in tumor microenvironment modulation and immune escape mechanisms. CONCLUSION: CNGB3 demonstrates significant potential for early detection and individualized management of gastric cancer. Despite limitations including a single-center database analysis and lack of multicenter clinical validation, CNGB3 warrants further investigation as a biomarker and potential therapeutic target. Core tip: Gastric cancer remains a leading cause of cancer mortality, and effective molecular biomarkers are needed to improve risk stratification. Through integrated multi-omics analysis, we identify CNGB3—a cyclic nucleotide-gated channel subunit—as a novel gastric cancer biomarker that is upregulated in tumors and linked to poor survival. Functional validation shows CNGB3 drives gastric cancer cell proliferation, migration, and metastasis in vitro. These results position CNGB3 as both a prognostic indicator and a candidate therapeutic target.

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Publication Details

Journal
Research Square
Published
2026-11-04
DOI
https://doi.org/10.21203/rs.3.rs-11338356/v1
Primary Topic
Gastric Cancer Management and Outcomes
Type
preprint
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preprint

CNGB3 promotes proliferation migration and metastasis in gastric cancer cells

Hangying Lin, Yun Lin, Shangzhe Zheng, Zhirong Yang
Research Square
Gastric Cancer Management and Outcomes
preprint

CNGB3 promotes proliferation migration and metastasis in gastric cancer cells

Hangying Lin, Yun Lin, Shangzhe Zheng, Zhirong Yang
preprint en

Abstract

Abstract AIM: To investigate CNGB3 as a prognostic biomarker and functional driver of gastric cancer progression. MATERIALS AND METHODS: We used multi-omics approaches to comprehensively evaluate CNGB3's role in gastric cancer. Transcriptomic and clinical data were retrieved from the TCGA, GTEx, and GEO (GSE84437) databases. Analyzed methods included differential expression analysis between tumor and normal tissues, functional enrichment analysis (GO, KEGG, GSEA), immune infiltration analysis using the ssGSEA algorithm, and Kaplan-Meier survival analysis with Cox regression modeling. RESULTS: CNGB3 expression levels in gastric cancer tissues were significantly elevated compared to normal tissues, and even higher in metastatic gastric cancer (p < 0.05). Differential expression analysis identified 2,059 differentially expressed genes (|log2FC| > 1), from which 20 hub genes were identified through PPI network construction. Immune infiltration analysis showed substantial differences in immune cell enrichment between high and low CNGB3 expression groups (p < 0.001), including elevated activated NK cells and CD8+ T cells, suggesting CNGB3 may influence gastric cancer immune evasion by modulating the tumor microenvironment. Kaplan-Meier survival analysis indicated that overall survival, disease-specific survival, and progression-free survival rates were markedly reduced in the high CNGB3 expression group compared to the low expression group (p < 0.05). These findings reveal for the first time CNGB3's role as a prognostic biomarker across cancer types. The association between CNGB3 expression and immune cell infiltration suggests its involvement in tumor microenvironment modulation and immune escape mechanisms. CONCLUSION: CNGB3 demonstrates significant potential for early detection and individualized management of gastric cancer. Despite limitations including a single-center database analysis and lack of multicenter clinical validation, CNGB3 warrants further investigation as a biomarker and potential therapeutic target. Core tip: Gastric cancer remains a leading cause of cancer mortality, and effective molecular biomarkers are needed to improve risk stratification. Through integrated multi-omics analysis, we identify CNGB3—a cyclic nucleotide-gated channel subunit—as a novel gastric cancer biomarker that is upregulated in tumors and linked to poor survival. Functional validation shows CNGB3 drives gastric cancer cell proliferation, migration, and metastasis in vitro. These results position CNGB3 as both a prognostic indicator and a candidate therapeutic target.

Research Square
Fujian Medical University (CN), Xiamen University (CN)
Gastric Cancer Management and Outcomes
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