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Loss of GGT6 promotes colorectal cancer progression and correlates with poor prognosis: a study based on
Yu Yang1, Jiamin Li1, Shangzhiyu Gong1
1Department of Oncology, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Gusu School, Nanjing Medical University, Suzhou, China.
Background:
Gamma-glutamyl transferase 6 (GGT6) belongs to the GGT family and its functional mechanisms in colorectal cancer (CRC) are still not well understood in the academic community. This study aims to fill this research gap by examining the clinical relevance and biological effects of GGT6.
Methods:
GGT6 expression and clinical data were integrated from The Cancer Genome Atlas (TCGA), Human Protein Atlas (HPA), and Gene Expression Omnibus (GEO) databases. Prognostic value was assessed using Kaplan-Meier (K-M) and Cox regression. Biological pathways and immune landscapes were analyzed via Gene Set Enrichment Analysis (GSEA), CIBERSORT, and Tumor Immune Dysfunction and Exclusion (TIDE). Findings were validated using tissue microarrays and in vitro assays, including Cell Counting Kit-8 (CCK-8), colony formation, and transwell assays in HT-29 and DLD-1 cell lines.
Results:
GGT6 was significantly downregulated in CRC tissues, and its low expression served as an independent prognostic factor for poor survival. Functional analysis linked GGT6 to peroxisome proliferator-activated receptor (PPAR), epithelial-mesenchymal transition (EMT), and KRAS signaling. Importantly, knockdown of GGT6 significantly promoted the proliferation, migration, and invasion of HT-29 and DLD-1 cells. Furthermore, GGT6 expression correlated with immune infiltration and predicted sensitivity to common therapeutic drugs.
Conclusions:
GGT6 acts as a tumor suppressor in CRC. Its downregulation promotes malignant progression and correlates with poor prognosis, making it a promising biomarker and potential therapeutic target.
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