PELO regulates erythroid differentiation through interaction with MYC to upregulate KLF10.

Jinglan Hao, Guiqin Han, Xin Liang, Yongtong Ruan, Chen Huang, Naer Sa, Hang Hu, Bixi Hu, Zhongqi Li, Kai Zhang, Ping Gao, Xiaoming Dong
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Abstract

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.

PELO 通过与 MYC 相互作用上调 KLF10 来调节红细胞分化。
红细胞生成是一个多步骤的红细胞生成过程,由多种调控因子控制。核糖体拯救因子 PELO 在细胞减数分裂和小鼠胚胎发育中起着至关重要的作用。然而,PELO 在红细胞分化中的功能仍不清楚。在这里,我们发现敲除 PELO 增加了海明诱导的 K562 和 HEL 细胞的红细胞分化,表现出更多的联苯胺阳性细胞和更高的红细胞基因 mRNA 水平。PELO 基因敲除抑制了 K562 细胞的增殖和细胞周期的进展,并促进了其凋亡。从机理上讲,PELO可通过与MYC相互作用来调控KLF10的表达。此外,KLF10的敲除还能增强hemin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,调控红细胞分化并提高KLF10的表达水平。
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