Department of General Surgery, Tangdu Hospital of the Fourth Military Medical University, Xi'an 710038, PR China.
Biochem Biophys Res Commun. 2012 Nov 16;428(2):210-5. doi: 10.1016/j.bbrc.2012.09.126. Epub 2012 Oct 1.
Recently, catecholamines have been described as being involved in the regulation of cancer genesis and progression. Here, we reported that adrenaline increased the cell proliferation and decreased the cisplatin induced apoptosis in HT29 cells. Further study found that adrenaline increased miR-155 expression in an NFκB dependent manner. HT29 cells overexpressing miR-155 had a higher cell growth rate and more resistance to cisplatin induced apoptosis. In contrast, HT29 cells overexpressing miR-155 inhibitor displayed decreased cell proliferation and sensitivity to cisplatin induced cell death. In summary, our study here revealed that adrenaline-NFκB-miR-155 pathway at least partially contributes to the psychological stress induced proliferation and chemoresistance in HT29 cells, shedding light on increasing the therapeutic strategies of cancer chemotherapy.
最近,儿茶酚胺被描述为参与癌症发生和进展的调节。在这里,我们报道肾上腺素增加了 HT29 细胞的细胞增殖,并减少了顺铂诱导的细胞凋亡。进一步的研究发现,肾上腺素以 NFκB 依赖的方式增加了 miR-155 的表达。过表达 miR-155 的 HT29 细胞具有更高的细胞生长速率和对顺铂诱导的细胞凋亡的更强抗性。相反,过表达 miR-155 抑制剂的 HT29 细胞显示出细胞增殖减少和对顺铂诱导的细胞死亡的敏感性增加。总之,我们的研究揭示了肾上腺素-NFκB-miR-155 通路至少部分导致了 HT29 细胞中应激诱导的增殖和化疗耐药性,为增加癌症化疗的治疗策略提供了线索。