ArticleNan fang yi ke da xue xue bao = Journal of Southern Medical University
[Phosphatidylinositol glycan anchor biosynthesis class T promotes malignant phenotype of colon cancer through the NF-κB signaling pathway].
Article in Nan fang yi ke da xue xue bao = Journal of Southern Medical University. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectivesTo explore the role of phosphatidylinositol glycan anchor biosynthesis class T (PIGT) in progression of colorectal cancer (CRC) and its molecular mechanism.
methodsThe differential expression of PIGT in CRC and adjacent normal tissues was analyzed using GEPIA, UALCAN and TNMplot databases. Quantitative PCR and Western blotting were used to detect PIGT expression levels in CRC cell lines HCT116 and HCT8 and in normal colorectal mucosal NCM460 cells. The correlation between PIGT expression and 10-year recurrence-free survival of CRC patients was evaluated using Kaplan-Meier survival analysis. In CRC cells, the effects of PIGT knockdown on cell proliferation, clonogenic ability, migration, invasion and angiogenesis capacity were assessed. The NF-κB signaling pathway was identified as a key downstream pathway using transcriptome sequencing and pathway enrichment analysis, and the expressions of NF-κB key proteins and epithelial-mesenchymal transition (EMT) markers were detected using Western blotting. LPS rescue experiments were performed to confirm the regulatory relationship between PIGT and the NF-κB pathway. A nude mouse subcutaneous xenograft model was used to verify the oncogenic role of PIGT
resultsPIGT was significantly upregulated in CRC tissues and cell lines. High PIGT expression was closely associated with a shorter recurrence-free survival in patients with stage II to IV CRC. In CRC cells, PIGT knockdown significantly inhibited cell proliferation, migration, invasion and angiogenesis and effectively reversed EMT. Downregulation of PIGT reduced the phosphorylation level of P65 and suppressed NF-κB pathway activation, and these changes were effectively reversed by LPS treatment. In the tumor-bearing mice, PIGT knockdown markedly reduced subcutaneous tumor growth.
conclusionsPIGT promotes CRC progression and EMT by activating the NF‑κB signaling pathway, suggesting the potential of PIGT as both a prognostic biomarker and a therapeutic target for CRC.
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