结肠癌干细胞是结肠癌浸润转移和复发主要原因之一。静息性Bmi1+结肠癌干细胞具有更强抗药性和致瘤潜能，低代谢是其显著特征，然静息性结肠癌干细胞低代谢分子机制尚不明确。我们先前研究鉴定了一群具有干细胞特性的CD44+CD58+结肠癌细胞，CD58是一个新的结肠癌干细胞分子识别标志，激活CD58促进了结肠癌干细胞自我更新。有趣的是，我们还发现表达或激活CD58明显抑制糖代谢关键限速酶HK2活性，提示CD58可能还参与调控结肠癌干细胞糖代谢过程，然CD58下调HK2分子机制尚不明了。本研究拟在先前基础上，在转录和蛋白质修饰水平明确原代和结肠癌细胞系中CD58通过下调HK2降低结肠癌干细胞糖代谢分子机制，探讨CD58靶向HK2降低糖代谢对结肠癌干细胞生物学功能的影响。本研究将肿瘤代谢与肿瘤干细胞相结合，对阐明CD58在结肠癌干细胞中的分子特征和生物学功能有重要意义，为结肠癌治疗提供新的潜在靶点。

colorectal cancer stem cells (CCSC) remaining is one of the main causes for recurrence and metastasis of colorectal cancer. Resting Bmi1+ CCSCs have stronger drug-resistance and tumorigenic potential, with the prominent feature of lower metabolism. However, the molecular mechanisms of lower metabolism in resting CCSCs remain unclear. Our previous studies have identified a group of CD44+CD58+ colorectal cancer cells with stem cell properties, indicating CD58 is a new molecular marker of CCSCs. CD58 activation promotes self-renewal of CCSCs. Interestingly, we also found that CD58 expression or activation significantly inhibited the activity of HK2, which is the main rate-limiting enzyme of glucose metabolism, indicating that CD58 may also be involved in the regulation of glucose metabolism in CCSCs. However, the molecular mechanism of CD58 down-regulating HK2 is still unknown. This study focuses on previous basis through the level of transcription and protein modification to identify the molecular mechanisms of CD58 reducing glucose metabolism by down-regulating HK2 in the primary and colorectal cancer cell lines; to investigate the effects of CD58 reduced glucose metabolism by targeting HK2 on the biological function of CCSCs. In this study, cancer metabolism is combined with cancer stem cells, which is important to elucidate the molecular characteristics and biological function of CD58 in CCSCs, providing new potential targets for colorectal cancer therapy in the future.