MiR‐214‐3p overexpression‐triggered chondroitin polymerizing factor (CHPF) inhibition modulates the ferroptosis and metabolism in colon cancer

下调和上调 基因沉默 结直肠癌 癌症研究 基因敲除 化学 免疫印迹 癌细胞 细胞生长 小干扰RNA 癌症 生物 生物化学 医学 内科学 转染 细胞凋亡 基因
作者
Zhiyuan Yun,Di Wu,Xin Wang,Peng Huang,Na Li
出处
期刊:Kaohsiung Journal of Medical Sciences [Wiley]
卷期号:40 (3): 244-254 被引量:1
标识
DOI:10.1002/kjm2.12802
摘要

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.

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