肿瘤内在型 FABP5 通过 HIF-1 信号通路成为结肠癌细胞生长的新驱动因子。
Tumor-intrinsic FABP5 is a novel driver for colon cancer cell growth via the HIF-1 signaling pathway.
机构信息
Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, South Korea; Department of Physiology, Seoul National University College of Medicine, Seoul 03080, South Korea; Faculty of Engineering, Yokohama National University, Yokohama 240-8501, Japan.
Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul 03080, South Korea; Department of Physiology, Seoul National University College of Medicine, Seoul 03080, South Korea.
出版信息
Cancer Genet. 2021 Nov;258-259:151-156. doi: 10.1016/j.cancergen.2021.11.001. Epub 2021 Nov 5.
Dysfunctional lipid metabolism is a known cause of cancer development and progression, yet little is known about the underlying molecular mechanisms that contribute to cancer progression. In this study, we demonstrate that fatty acid binding protein 5 (FABP5) is elevated in colon cancer tissue and this increased expression is linked to upregulation of the hypoxia-inducible factor-1 (HIF-1) signaling pathway. Under physiologically in vivo mimicked conditions via a polydimethylsiloxane (PDMS)-based three-dimensional (3D) culture chip, FABP5-knockdown colon cancer cells exhibited attenuated cell growth throughout the culture period. FABP5 was found to regulate HIF-1α protein levels and gene expression levels within the HIF-1α signaling pathway under hypoxic conditions. Our results provide evidence that supports the use of FABP5 as a prognostic factor in colon cancer. The FABP5/HIF-1α axis is a promising target for ameliorating fatty acid-triggered cancer progression.
脂质代谢功能障碍是癌症发生和发展的已知原因，但对于导致癌症进展的潜在分子机制知之甚少。在这项研究中，我们证明脂肪酸结合蛋白 5（FABP5）在结肠癌组织中升高，这种表达增加与缺氧诱导因子 1（HIF-1）信号通路的上调有关。在聚二甲基硅氧烷（PDMS）基三维（3D）培养芯片上模拟生理体内的条件下，FABP5 敲低的结肠癌细胞在整个培养期间表现出细胞生长减弱。在低氧条件下，发现 FABP5 调节 HIF-1α 信号通路中的 HIF-1α 蛋白水平和基因表达水平。我们的结果提供了支持将 FABP5 用作结肠癌预后因素的证据。FABP5/HIF-1α 轴是改善脂肪酸触发的癌症进展的有前途的靶标。
Zotero 插件