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<p>KIN17 is a DNA- and RNA-binding protein involved in the regulation of several human cancers. However, its role in cancer progression and metastasis in cholangiocarcinoma remains largely unknown. In this work, the expression of KIN17 in CCA patients was investigated using bioinformatics and immunohistochemical staining. The effects of KIN17 on CCA cells’ migration and invasion were examined by scratch assay and transwell assay. In RBE and HCCC-9810 cells, knockdown of KIN17 significantly suppressed the migration and invasion ability of the cells and also inhibited the mTOR pathway, while overexpression of KIN17 promoted the migration and invasion ability of HUCCT-1 cells and stimulated the mTOR pathway, as well as genes involved in epithelial-mesenchymal transition. These findings indicate that expression of KIN17 in CCA is abnormal compared to the normal conditions and promotes the invasion and migration of CCA cells. Meanwhile, we hypothesize that KIN17 affects the migration and invasion of CCA cells through the regulation of mTOR and EMT signaling pathways. Hence, we propose KIN17 to be a novel diagnostic biomarker and therapeutic target for CCA.</p>

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Regulation of EMT and cholangiocarcinoma metastasis by KIN17 through the mTOR signaling pathway

  • 期刊论文

  • 发表日期：

    2026年4月11日

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  • Yuxia Yang,
  • Qianying Luo,
  • Chuhong Huang,
  • Xiaocong Lin,
  • Lok Ting Chu,
  • Qiuyan Li,
  • Jinjing Tang,
  • Tao Zeng

摘要

KIN17 is a DNA- and RNA-binding protein involved in the regulation of several human cancers. However, its role in cancer progression and metastasis in cholangiocarcinoma remains largely unknown. In this work, the expression of KIN17 in CCA patients was investigated using bioinformatics and immunohistochemical staining. The effects of KIN17 on CCA cells’ migration and invasion were examined by scratch assay and transwell assay. In RBE and HCCC-9810 cells, knockdown of KIN17 significantly suppressed the migration and invasion ability of the cells and also inhibited the mTOR pathway, while overexpression of KIN17 promoted the migration and invasion ability of HUCCT-1 cells and stimulated the mTOR pathway, as well as genes involved in epithelial-mesenchymal transition. These findings indicate that expression of KIN17 in CCA is abnormal compared to the normal conditions and promotes the invasion and migration of CCA cells. Meanwhile, we hypothesize that KIN17 affects the migration and invasion of CCA cells through the regulation of mTOR and EMT signaling pathways. Hence, we propose KIN17 to be a novel diagnostic biomarker and therapeutic target for CCA.