Scholarlink

<p>Peptidylprolyl isomerase like 1 (PPIL1) is a component of the Prp19 complex (Prp19C), which plays a crucial role in spliceosome assembly. However, the role of PPIL1 in hepatocellular carcinoma (HCC) progression remains unclear. Analysis of TCGA and LIRI-JP datasets revealed that elevated expression of components from the Prp19 complex (Prp19C) is associated with poor prognosis in HCC. PPIL1, which significantly exacerbated tumor progression in this complex, would be a promising therapy target. To investigate the effect of PPIL1 on HCC cells, CCK-8, colony formation, and sphere-formation assays were performed to evaluate its influence on proliferation. Wound healing and Transwell assays were conducted to assess migration and invasion capabilities. The results demonstrated that knockdown of PPIL1 significantly attenuated the malignant phenotype of HCC cells by reducing their capability for proliferation, as well as by diminishing their potential for migration, invasion, and stemness. Flow cytometry analysis demonstrated that PPIL1 knockdown induces G2/M phase cell cycle arrest in HCC cells. Western blot analysis showed that knockdown of PPIL1 significantly suppressed the mTOR/ERK/NF-κB signaling cascade and the expression of CHK2. Overall, our results demonstrated that PPIL1 is highly expressed in HCC tissues and is associated with poor prognosis. Functionally, PPIL1 drives the malignant phenotype of HCC cells and modulates the mTOR/ERK/NF-κB pathway and the expression of CHK2.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

PPIL1 promotes hepatocellular carcinoma progression and associates with poor prognosis

  • 期刊论文

  • 发表日期：

    2026年1月13日

查看全文
  • Yunyu Wu,
  • Shuqing Jiang,
  • Junming Yu,
  • Hechun Lin,
  • Saihua Zhang,
  • Yizi Jin,
  • Yang Su,
  • Wenjiao Jin,
  • Chao Ge,
  • Qin Geng,
  • Taoyang Chen,
  • Jinjun Li,
  • Lin Mao,
  • Hong Li

摘要

Peptidylprolyl isomerase like 1 (PPIL1) is a component of the Prp19 complex (Prp19C), which plays a crucial role in spliceosome assembly. However, the role of PPIL1 in hepatocellular carcinoma (HCC) progression remains unclear. Analysis of TCGA and LIRI-JP datasets revealed that elevated expression of components from the Prp19 complex (Prp19C) is associated with poor prognosis in HCC. PPIL1, which significantly exacerbated tumor progression in this complex, would be a promising therapy target. To investigate the effect of PPIL1 on HCC cells, CCK-8, colony formation, and sphere-formation assays were performed to evaluate its influence on proliferation. Wound healing and Transwell assays were conducted to assess migration and invasion capabilities. The results demonstrated that knockdown of PPIL1 significantly attenuated the malignant phenotype of HCC cells by reducing their capability for proliferation, as well as by diminishing their potential for migration, invasion, and stemness. Flow cytometry analysis demonstrated that PPIL1 knockdown induces G2/M phase cell cycle arrest in HCC cells. Western blot analysis showed that knockdown of PPIL1 significantly suppressed the mTOR/ERK/NF-κB signaling cascade and the expression of CHK2. Overall, our results demonstrated that PPIL1 is highly expressed in HCC tissues and is associated with poor prognosis. Functionally, PPIL1 drives the malignant phenotype of HCC cells and modulates the mTOR/ERK/NF-κB pathway and the expression of CHK2.