Abstract：
Colon cancer is a common cancer with high mortality globally. The role of chondroitin polymerizing factor (CHPF) has been elucidated in various cancers. However, its role and mechanism remain unknown in colon cancer. CHPF expression was examined by GEPIA database, reverse transcription-quantitative polymerase chain reaction and western blot. The relationship between CHPF expression and the clinicopathologic characteristics as well as miR-214-3p level was determined in colon cancer patients. The role and mechanism of CHPF in the growth, ferroptosis, and glycolysis of colon cancer cells were evaluated by cell counting kit-8, biochemical detections, luciferase, and western blot experiments. Additionally, the role of CHPF was explored in xenografted mice. CHPF expression was increased and was related to advanced TNM stage, poor differentiation and shorter overall survival in patients with colon cancer. Knockdown of CHPF inhibited colon cancer cell growth, and downregulated the expression of proteins involving in ferroptosis and glycolysis both in vitro and in vivo. Besides, CHPF silencing increased the levels of ferrous iron and ROS, but decreased glucose uptake, lactate product, and ATP level in vitro. Mechanically, miR-214-3p directly targeted CHPF and negatively regulated its expression. Upregulation of miR-214-3p reduced cell viability, glucose uptake, lactate product, and ATP level, but increased the levels of ferrous iron and ROS, which were reversed by the overexpression of CHPF. Upregulation of CHPF predicted poor prognosis, and miR-214-3p/CHPF axis inhibited growth, downregulated the levels of glycolysis-related indexes, and promoted ferroptosis in colon cancer cells.
摘要：
结肠癌是全球常见的高死亡率癌症。软骨素聚合因子（CHPF）在各种癌症中的作用已得到阐明。然而,其在结肠癌中的作用和机制尚不清楚。CHPF表达由GEPIA数据库检测，逆转录-定量聚合酶链反应和蛋白质印迹。在结肠癌患者中确定CHPF表达与临床病理特征以及miR-214-3p水平之间的关系。CHPF在其生长中的作用及机制,铁性凋亡,细胞计数试剂盒-8,生化检测,荧光素酶,和蛋白质印迹实验。此外,研究了CHPF在异种移植小鼠中的作用.CHPF表达增加，与晚期TNM分期有关，结肠癌患者分化差，总生存期较短。CHPF敲除抑制结肠癌细胞生长，并在体外和体内下调参与铁凋亡和糖酵解的蛋白质的表达。此外,CHPF沉默增加了亚铁和ROS的水平，但降低了葡萄糖的摄取，乳酸产品，和体外ATP水平。机械上,miR-214-3p直接靶向CHPF并负调控其表达。miR-214-3p上调降低细胞活力，葡萄糖摄取，乳酸产品，和ATP水平，但是增加了亚铁和活性氧的水平，通过CHPF的过表达而逆转。CHPF上调预测预后不良，miR-214-3p/CHPF轴抑制生长，下调糖酵解相关指标的水平，并促进结肠癌细胞的铁凋亡。
