南方医科大学学报 ›› 2026, Vol. 46 ›› Issue (9): 2173-2184.doi: 10.12122/j.issn.1673-4254.2026.09.16

• • 上一篇    

磷脂酰肌醇聚糖锚定生物合成T类经由 NF-κB 通路调控上皮间质转化并促进结直肠癌恶性进展

李百超1(), 王炳哲1, 梅向辉1, 田野1, 韩亮1, 张九娜2()   

  1. 1.河北工程大学临床医学院,河北 邯郸 056000
    2.河北工程大学附属医院消化内科,河北 邯郸 056000
  • 收稿日期:2025-12-25 出版日期:2026-09-20 发布日期:2026-09-30
  • 通讯作者: 张九娜 E-mail:1832492339@qq.com;shitouli1020@163.com
  • 作者简介:李百超,在读硕士研究生,E-mail: 1832492339@qq.com
  • 基金资助:
    河北省自然科学基金(H2022402009);河北省省级科技计划项目(ZF2023221)

Phosphatidylinositol glycan anchor biosynthesis class T promotes malignant phenotype of colon cancer through the NF-κB signaling pathway

Baichao LI1(), Bingzhe WANG1, Xianghui MEI1, Ye TIAN1, Liang HAN1, Jiuna ZHANG2()   

  1. 1.School of Clinical Medicine, Hebei University of Engineering, Handan 056000, China
    2.Department of Gastroenterology, Affiliated Hospital of Hebei University of Engineering, Handan 056000, China
  • Received:2025-12-25 Online:2026-09-20 Published:2026-09-30
  • Contact: Jiuna ZHANG E-mail:1832492339@qq.com;shitouli1020@163.com

摘要:

目的 探讨磷脂酰肌醇聚糖锚定生物合成T类(PIGT)在结直肠癌进展中的生物学功能及相关分子机制。 方法 利用数据库GEPIA、UALCAN、TNMplot分析PIGT在结直肠癌组织与配对正常组织中的表达差异;通过qPCR及Western blotting在结直肠癌细胞系(HCT116,HCT8)与正常结直肠黏膜细胞系(NCM460)中验证其表达水平。利用Kaplan-Meier plotter数据库,探究PIGT表达与结直肠癌患者10年无复发生存期(RFS)的关联。采用质粒转染技术在HCT116、 HCT8细胞中敲低PIGT,结合集落形成实验、软琼脂克隆实验、Transwell迁移及侵袭实验、伤口愈合实验及体外血管形成实验,评估PIGT对结直肠癌细胞增殖、克隆形成、迁移、侵袭及血管生成能力的影响;基于敲低组与对照组的转录组测序及通路富集结果,选定NF-κB通路进行验证,并通过Western blotting检测敲低PIGT后NF-κB通路关键蛋白(P-P65、P65)及上皮-间质转化(EMT)相关标志物(E-cadherin、N-cadherin、Vimentin、MMP9、VEGF-C)的表达变化,通过脂多糖恢复实验进一步分析其通路调控关系;构建裸鼠皮下荷瘤模型,将PIGT敲低组与对照组HCT116细胞分别接种于裸鼠背部皮下,取瘤后测量肿瘤重量,观察PIGT敲低对体内肿瘤生长的影响。 结果 公共数据库(TNMplot、UALCAN、GEPIA)分析及细胞水平验证显示,PIGT在结直肠癌组织及细胞系中均高表达(P<0.05)。Kaplan-Meier plotter数据库生存分析显示,中晚期(Ⅱ~Ⅳ期)结直肠癌患者中,PIGT高表达者的无复发生存期缩短(P<0.05)。功能实验证实,敲低PIGT可抑制结直肠癌细胞的增殖、克隆形成、迁移、侵袭及体外血管生成能力(P<0.05);同时上调上皮标志物E-cadherin表达,下调间质标志物N-cadherin、Vimentin、MMP9、VEGF-C的表达,从而逆转上皮间质转化进程(P<0.05)。在机制层面,转录组测序及通路富集分析显示NF-κB信号通路在PIGT敲低后下调;Western blotting验证显示,PIGT敲低组NF-κB通路关键蛋白P-P65的磷酸化水平降低(P<0.05),脂多糖恢复实验可逆转 PIGT 敲低所致的 NF-κB 通路抑制及 EMT 相关蛋白异常表达。裸鼠体内荷瘤实验结果显示,与对照组相比,PIGT敲低组裸鼠皮下肿瘤的质量降低(P<0.05)。 结论 PIGT在结直肠癌中异常高表达,可能通过影响NF-κB信号通路促进结直肠癌细胞增殖、迁移、侵袭及EMT进程,有望成为结直肠癌潜在的预后生物标志物及靶向治疗靶点。

关键词: 结直肠癌, 磷脂酰肌醇聚糖锚定生物合成T类, NF-κB, 上皮-间质转化

Abstract:

Objective 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. Conclusion 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.

Key words: colorectal neoplasms, phosphatidylinositol glycan anchor biosynthesis class T, nuclear factor-κB, epithelial-mesenchymal transition