DataSheet_1_EPHX2 Inhibits Colon Cancer Progression by Promoting Fatty Acid Degradation.xlsx

Tumor cells use metabolic reprogramming to keep up with the need for bioenergy, biosynthesis, and oxidation balance needed for rapid tumor division. This phenomenon is considered a marker of tumors, including colon cancer (CRC). As an important pathway of cellular energy metabolism, fatty acid metabolism plays an important role in cellular energy supply and oxidation balance, but presently, our understanding of the exact role of fatty acid metabolism in CRC is limited. Currently, no lipid metabolism therapy is available for the treatment of CRC. The establishment of a lipidmetabolism model regulated by oncogenes/tumor suppressor genes and associated with the clinical characteristics of CRC is necessary to further understand the mechanism of fatty acid metabolism in CRC. In this study, through multi-data combined with bioinformatic analysis and basic experiments, we introduced a tumor suppressor gene, EPHX2, which is rarely reported in CRC, and confirmed that its inhibitory effect on CRC is related to fatty acid degradation.

肿瘤细胞通过代谢重编程，以满足快速增殖所需的生物能量供给、生物合成过程及氧化平衡需求。该现象被视为包括结直肠癌（Colon Cancer, CRC）在内的各类肿瘤的标志物。作为细胞能量代谢的重要通路，脂肪酸代谢在细胞能量供给与氧化平衡中发挥关键作用，但目前学界对脂肪酸代谢在结直肠癌中的确切作用仍认识有限。目前尚无用于结直肠癌治疗的脂质代谢疗法。为进一步阐明脂肪酸代谢在结直肠癌中的作用机制，亟需构建由致癌基因/抑癌基因调控且与结直肠癌临床特征相关联的脂质代谢模型。本研究通过多源数据联合生物信息学分析与基础实验，报道了一种在结直肠癌中鲜有研究的抑癌基因EPHX2，并证实其对结直肠癌的抑制作用与脂肪酸降解过程密切相关。