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The miR-145-5p/CD36 pathway mediates PCB2-induced apoptosis in MCF-7 cells
Yuan Yuan,Caihua Xue,Qiang Wu,Mengjie Wang,Jiahua Liu,Longfei Zhang,Qianwen Xing,Jingyan Liang,Hua Wu,Zhi Chen 한국유전학회 2021 Genes & Genomics Vol.43 No.2
Background Procyanidin B2 (PCB2) can increase the levels of anti-infammatory and immune mediators. Objectives However, its molecular mechanism in human breast cancer remains unclear. This study aimed to investigate the antitumor efect of PCB2 on MCF-7 cells and to examine the underlying mechanism. Methods The fow cytometry and EdU incorporation assays were measured the PCB2-induced BMECs. The expression levels of infammatory factors and immune response genes were upregulated in MCF-7 cells, high-throughput sequencing was used to detect diferentially expressed genes in blank and PCB2-treated MCF-7 cells. Results The results showed that PCB2 induced the apoptosis of MCF-7 cells. CD36 profles were afected in MCF-7 cells. Additionally, prediction software identifed a miR-145-5p binding site in the CD36 sequence. Luciferase reporter assays and Western blot analysis were used to verify the regulatory relationships between the diferentially expressed miRNA miR145-5p and CD36. MiR-145-5p and its key target (CD36) constitute a potential miRNA-mRNA regulatory pair. Functional studies in MCF-7 cells revealed that CD36 promotes but miR-145-5p inhibits apoptosis. Conclusion Overall, these data suggest that miR-145-5p inhibits the enhancing efect of PCB2 on CD36 expression by binding CD36 and subsequently regulating apoptosis, the immune response and anti-infammatory pathways. These results provide theoretical and experimental support for the treatment of breast cancer.
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Hongliang Li,Yue Zhou,Yongqi Yang,Yiwen Zha,Bingqian Ye,Seo-Yeong Mun,Wenwen Zhuang,Jingyan Liang,Won Sun Park The Korean Society of Pharmacology 2023 The Korean Journal of Physiology & Pharmacology Vol.27 No.4
Voltage-dependent K<sup>+</sup> (Kv) channels are widely expressed on vascular smooth muscle cells and regulate vascular tone. Here, we explored the inhibitory effect of encainide, a class Ic anti-arrhythmic agent, on Kv channels of vascular smooth muscle from rabbit coronary arteries. Encainide inhibited Kv channels in a concentration-dependent manner with an IC<sub>50</sub> value of 8.91 ± 1.75 μM and Hill coefficient of 0.72 ± 0.06. The application of encainide shifted the activation curve toward a more positive potential without modifying the inactivation curve, suggesting that encainide inhibited Kv channels by altering the gating property of channel activation. The inhibition by encainide was not significantly affected by train pulses (1 and 2 Hz), indicating that the inhibition is not use (state)-dependent. The inhibitory effect of encainide was reduced by pretreatment with the Kv1.5 subtype inhibitor. However, pretreatment with the Kv2.1 subtype inhibitor did not alter the inhibitory effects of encainide on Kv currents. Based on these results, encainide inhibits vascular Kv channels in a concentration-dependent and use (state)-independent manner by altering the voltage sensor of the channels. Furthermore, Kv1.5 is the main Kv subtype involved in the effect of encainide.
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