College of Life Sciences, Shaanxi Normal University, Xi'an, China.
Hansoh Bio, 9600 Medical Center drive, Rockville, USA.
FEBS J. 2024 Nov;291(21):4714-4731. doi: 10.1111/febs.17254. Epub 2024 Aug 29.
Erythropoiesis is a multistep process of erythroid cell production that is controlled by multiple regulatory factors. Ribosome rescue factor PELO plays a crucial role in cell meiotic division and mice embryonic development. However, the function of PELO in erythroid differentiation remains unclear. Here, we showed that knockdown of PELO increased hemin-induced erythroid differentiation of K562 and HEL cells, exhibiting a higher number of benzidine-positive cells and increased mRNA levels of erythroid genes. PELO knockdown inhibited the proliferation and cell cycle progression and promoted apoptosis of K562 cells. Mechanistically, PELO could regulate the expression of KLF10 through interaction with MYC. Moreover, KLF10 knockdown also enhanced erythroid differentiation of K562 and HEL cells induced by hemin. Collectively, our results demonstrated that PELO regulates erythroid differentiation and increases KLF10 expression levels by interacting with MYC.
红细胞生成是一个多步骤的红细胞生成过程,受多种调节因子控制。核糖体拯救因子 PELO 在细胞减数分裂和小鼠胚胎发育中发挥着关键作用。然而,PELO 在红细胞分化中的功能尚不清楚。在这里,我们发现敲低 PELO 增加了 K562 和 HEL 细胞中海因诱导的红细胞分化,表现为更多的联苯胺阳性细胞和红细胞基因的 mRNA 水平增加。PELO 敲低抑制了 K562 细胞的增殖和细胞周期进程,并促进了细胞凋亡。在机制上,PELO 可以通过与 MYC 相互作用来调节 KLF10 的表达。此外,KLF10 的敲低也增强了海因诱导的 K562 和 HEL 细胞的红细胞分化。总之,我们的研究结果表明,PELO 通过与 MYC 相互作用来调节红细胞分化和增加 KLF10 的表达水平。