Shin Eun Ah, Sohn Eun Jung, Won Gunho, Yun Sangwook, Kim Jihyun, Kim Sung-hoon
College of Korean Medicine, Kyung Hee University, 1 Hoegi-dong, Dongdaemun-gu, Seoul, 130-701, South Korea.
In Vitro Cell Dev Biol Anim. 2016 Apr;52(4):473-8. doi: 10.1007/s11626-015-9985-9. Epub 2015 Dec 29.
Though special AT-rich sequence-binding protein 2 (SATB2) is reported as a transcriptional regulator of skeletal development and osteogenic differentiation, the underlying mechanism of SATB2 is not fully understood. Herein, we report that SATB2 is localized to the mitotic microtubules, the centrosome, and midbodies in mitotic cells with alpha-tubulin. Moreover, siRNA-mediated disruption of SATB2 in H460 cells caused the defect of nuclear morphology and multinucleate cells. SATB2 siRNA knockdown reduced the viability and downregulated the CDK2 expression in SKOV3 cells. Consistently, cell cycle analysis demonstrated that the silencing of SATB2 induced cell-cycle G1 arrest. Furthermore, proteosomal inhibitor MG132 treatment rescued the downregulation of CDK2 in SATB2-silenced SKOV3 cells. Taken together, our findings suggest that SATB2 regulates the mitosis of cell cycle and affects G1 cell cycle via interaction with CDK2.
尽管特殊富含AT序列结合蛋白2（SATB2）被报道为骨骼发育和成骨分化的转录调节因子，但其潜在机制尚未完全明确。在此，我们报告SATB2定位于有丝分裂细胞中的有丝分裂微管、中心体和中体，并与α-微管蛋白共定位。此外，siRNA介导的H460细胞中SATB2的破坏导致核形态缺陷和多核细胞。SATB2 siRNA敲低降低了SKOV3细胞的活力并下调了CDK2的表达。一致地，细胞周期分析表明SATB2的沉默诱导细胞周期G1期阻滞。此外，蛋白酶体抑制剂MG132处理挽救了SATB2沉默的SKOV3细胞中CDK2的下调。综上所述，我们的研究结果表明SATB2通过与CDK2相互作用调节细胞周期的有丝分裂并影响G1期细胞周期。
