College of Korean Medicine, Kyung Hee University, Seoul 02447, Korea.
Int J Mol Sci. 2022 Jun 9;23(12):6461. doi: 10.3390/ijms23126461.
Though cinnamaldehyde derivative (CB-PIC), a major compound of cinnamon, is known to have anticancer activity, its underlying mechanism is not fully understood. In the present study, the anticancer mechanism of CB-PIC was investigated in human hepatocellular carcinoma cells (HCCs) in association with signal transducer and activator of transcription 3 (STAT3) signaling. CB-PIC exerted cytotoxicity in HepG2 and Huh7 cells. CB-PIC increased the sub G1 population and attenuated the expression of pro-poly (ADP-ribose) polymerase (PARP) and pro-Caspase3 in HepG2 and Huh7 cells. Interestingly, CB-PIC significantly abrogated the expression of a glycolytic enzyme pyruvate kinase M2 (PKM2) in HepG2 cells more than in LNCaP, A549, and HCT-116 cells. Consistently, CB-PIC reduced the expression of hexokinase 2 (HK2) and PKM2, along with a reduced production of lactate in HepG2 and Huh7 cells. Notably, CB-PIC suppressed the phosphorylation of STAT3 in HepG2 and Huh7 cells and conversely STAT3 depletion enhanced the capacity of CB-PIC to suppress the expression of HK2, PKM2, and pro-caspase3 and to reduce the viability in Huh7 cells. Furthermore, CB-PIC activated the phosphorylation of AMPK and ERK and suppressed expression of IL-6 as STAT3-related genes in HepG2 and Huh7 cells. Conversely, pyruvate treatment reversed the inhibitory effect of CB-PIC on p-STAT3, HK2, PKM2, and pro-PARP in Huh7 cells. Overall, there findings suggest that CB-PIC exerts an apoptotic effect via inhibition of the Warburg effect mediated by p-STAT3 and pyruvate signaling.
虽然肉桂醛衍生物(CB-PIC)是肉桂的主要化合物,已知具有抗癌活性,但它的作用机制尚未完全阐明。在本研究中,研究了 CB-PIC 与信号转导和转录激活因子 3(STAT3)信号相关联在人肝癌细胞(HCCs)中的抗癌机制。CB-PIC 在 HepG2 和 Huh7 细胞中表现出细胞毒性。CB-PIC 增加了 sub G1 群体,并减弱了 HepG2 和 Huh7 细胞中多聚(ADP-核糖)聚合酶(PARP)前体和前 Caspase3 的表达。有趣的是,CB-PIC 显著下调了 HepG2 细胞中糖酵解酶丙酮酸激酶 M2(PKM2)的表达,而在 LNCaP、A549 和 HCT-116 细胞中则不然。一致地,CB-PIC 降低了 HepG2 和 Huh7 细胞中己糖激酶 2(HK2)和 PKM2 的表达,同时降低了乳酸的产生。值得注意的是,CB-PIC 抑制了 HepG2 和 Huh7 细胞中 STAT3 的磷酸化,而 STAT3 的耗竭增强了 CB-PIC 抑制 HK2、PKM2 和前 Caspase3 的表达并降低 Huh7 细胞活力的能力。此外,CB-PIC 激活了 HepG2 和 Huh7 细胞中 AMPK 和 ERK 的磷酸化,并抑制了 STAT3 相关基因 IL-6 的表达。相反,丙酮酸处理逆转了 CB-PIC 对 Huh7 细胞中 p-STAT3、HK2、PKM2 和前 PARP 的抑制作用。总之,这些发现表明,CB-PIC 通过抑制 p-STAT3 和丙酮酸信号介导的Warburg 效应发挥凋亡作用。