Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
[Phosphatidylinositol glycan anchor biosynthesis class T promotes malignant phenotype of colon cancer through the NF-κB signaling pathway].
Аннотация на английскомСтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Li Baichao, Wang Bingzhe, Mei Xianghui, Tian Ye, Han Liang, Zhang Jiuna
Аннотация
OBJECTIVES: To explore the role of phosphatidylinositol glycan anchor biosynthesis class T (PIGT) in progression of colorectal cancer (CRC) and its molecular mechanism.
METHODS: The 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 in vivo.
RESULTS: PIGT 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.
CONCLUSIONS: PIGT 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.
METHODS: The 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 in vivo.
RESULTS: PIGT 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.
CONCLUSIONS: PIGT 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.