Molecular and Cellular Oncology Laboratory, Department of Biochemistry, School of Life Sciences, University of Hyderabad, Hyderabad-500046, India.
J Biol Chem. 2012 Feb 17;287(8):5600-14. doi: 10.1074/jbc.M111.289843. Epub 2011 Dec 20.
Pre-B-cell leukemia homeobox interacting protein 1 or human PBX1 interacting protein (PBXIP1/HPIP) is a co-repressor of pre-B-cell leukemia homeobox 1 (PBX1) and is also known to regulate estrogen receptor functions by associating with the microtubule network. Despite its initial discovery in the context of hematopoietic cells, little is yet known about the role of HPIP in hematopoiesis. Here, we show that lentivirus-mediated overexpression of HPIP in human CD34(+) cells enhances hematopoietic colony formation in vitro, whereas HPIP knockdown leads to a reduction in the number of such colonies. Interestingly, erythroid colony number was significantly higher in HPIP-overexpressing cells. In addition, forced expression of HPIP in K562 cells, a multipotent erythro-megakaryoblastic leukemia cell line, led to an induction of erythroid differentiation. HPIP overexpression in both CD34(+) and K562 cells was associated with increased activation of the PI3K/AKT pathway, and corresponding treatment with a PI3K-specific inhibitor, LY-294002, caused a reduction in clonogenic progenitor number in HPIP-expressing CD34(+) cells and decreased K562 cell differentiation. Combined, these findings point to an important role of the PI3K/AKT pathway in mediating HPIP-induced effects on the growth and differentiation of hematopoietic cells. Interestingly, HPIP gene expression was found to be induced in K562 cells in response to erythroid differentiation signals such as DMSO and erythropoietin. The erythroid lineage-specific transcription factor GATA1 binds to the HPIP promoter and activates HPIP gene transcription in a CCCTC-binding factor (CTCF)-dependent manner. Co-immunoprecipitation and co-localization experiments revealed the association of CTCF with GATA1 indicating the recruitment of CTCF/GATA1 transcription factor complex onto the HPIP promoter. Together, this study provides evidence that HPIP is a target of GATA1 and CTCF in erythroid cells and plays an important role in erythroid differentiation by modulating the PI3K/AKT pathway.
前 B 细胞白血病同源盒相互作用蛋白 1 或人 PBX1 相互作用蛋白(PBXIP1/HPIP)是前 B 细胞白血病同源盒 1(PBX1)的共抑制因子,也已知通过与微管网络结合来调节雌激素受体功能。尽管它最初是在造血细胞的背景下发现的,但关于 HPIP 在造血中的作用知之甚少。在这里,我们表明,在人 CD34(+)细胞中通过慢病毒介导过表达 HPIP 可增强体外造血集落的形成,而 HPIP 敲低导致此类集落的数量减少。有趣的是,在过表达 HPIP 的细胞中,红细胞集落的数量明显更高。此外,在 K562 细胞(一种多能红巨核母细胞白血病细胞系)中强制表达 HPIP 导致红细胞分化的诱导。在 CD34(+)和 K562 细胞中过表达 HPIP 与 PI3K/AKT 通路的激活增加有关,用 PI3K 特异性抑制剂 LY-294002 处理相应的细胞会导致表达 HPIP 的 CD34(+)细胞中的集落形成祖细胞数量减少,并降低 K562 细胞分化。综合这些发现表明,PI3K/AKT 通路在介导 HPIP 对造血细胞生长和分化的影响方面起着重要作用。有趣的是,发现 HPIP 基因表达在 K562 细胞中响应于红细胞分化信号(如 DMSO 和促红细胞生成素)而被诱导。红细胞谱系特异性转录因子 GATA1 结合到 HPIP 启动子上,并以 CTCF 依赖性方式激活 HPIP 基因转录。共免疫沉淀和共定位实验显示 CTCF 与 GATA1 的关联表明 CTCF/GATA1 转录因子复合物被募集到 HPIP 启动子上。总之,这项研究提供了证据表明 HPIP 是红细胞中 GATA1 和 CTCF 的靶标,并通过调节 PI3K/AKT 通路在红细胞分化中发挥重要作用。