结直肠癌（CRC）是癌症相关死亡的第二大常见原因，是一个严重的全球健康问题。结直肠癌转移降低了癌症患者的生存率，强调需要确定新型抗癌药物和治疗靶点。在这里，我们介绍 Plectalibertellenone A (B) 作为一种有前途的抑制 CRC 细胞运动和葡萄糖代谢的药物，并探讨其在 CRC 细胞中的作用机制。 Plectalibertellenone A 抑制 TGF-β 基因表达和 TGF-β/Smad 信号通路的激活，通过调节 EMT 标记物和转录因子（如 E-cadherin、N-cadherin）的表达来逆转上皮间质转化 (EMT) 、波形蛋白、Slug、Snail、Twist 和 ZEB1/2。此外，Wnt信号传导的破坏抑制了CRC运动和葡萄糖代谢，包括糖酵解和氧化磷酸化，主要影响缺氧条件下的糖酵解酶、GLUT1、HK2、PKM2、LDHA和HIF-1α。因此，Plectalibertellenone A 是一种潜在的候选药物，可以开发成一种有前景的抗癌治疗方法，以预防 CRC 转移和抑制葡萄糖代谢。© 2024 国际生物化学与分子生物学联合会。

Colorectal cancer (CRC) is the second most common cause of cancer-related death and represents a serious worldwide health problem. CRC metastasis decreases the survival rate of cancer patients, underscoring the need to identify novel anticancer agents and therapeutic targets. Here, we introduce Plectalibertellenone A (B) as a promising agent for the inhibition of CRC cell motility and glucose metabolism and explore its mechanism of action in CRC cells. Plectalibertellenone A suppressed TGF-β gene expression and the activation of the TGF-β/Smad signaling pathway, leading to reverse epithelial to mesenchymal transition (EMT) by modulating the expressions of EMT markers and transcriptional factors such as E-cadherin, N-cadherin, vimentin, Slug, Snail, Twist, and ZEB1/2. Furthermore, disruption of Wnt signaling inhibited CRC motility and glucose metabolism including glycolysis and oxidative phosphorylation, primarily affecting glycolytic enzymes, GLUT1, HK2, PKM2, LDHA, and HIF-1α under hypoxic condition. Therefore, Plectalibertellenone A is a potential drug candidate that can be developed into a promising anticancer treatment to prevent CRC metastasis and inhibit glucose metabolism.© 2024 International Union of Biochemistry and Molecular Biology.