转录调节因子HMGA2促进胶质母细胞瘤的干性和致瘤性。
The transcriptional modulator HMGA2 promotes stemness and tumorigenicity in glioblastoma.
作者信息
Kaur Harpreet, Ali Sabeen Zulfiqar, Huey Lauren, Hütt-Cabezas Marianne, Taylor Isabella, Mao Xing-Gang, Weingart Melanie, Chu Qian, Rodriguez Fausto J, Eberhart Charles G, Raabe Eric H
机构信息
Division of Neuropathology and Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD 21287, USA; Division of Pediatric Oncology, Johns Hopkins University, Bloomberg Children's Hospital, Room 11379, 1800 Orleans St, Baltimore, MD 21287, USA.
Division of Neuropathology and Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University, Baltimore, MD 21287, USA.
出版信息
Cancer Lett. 2016 Jul 10;377(1):55-64. doi: 10.1016/j.canlet.2016.04.020. Epub 2016 Apr 18.
Glioblastoma (GBM) contains a population of stem-like cells that promote tumor invasion and resistance to therapy. Identifying and targeting stem cell factors in GBM may lead to the development of more effective therapies. High Mobility Group AT-hook 2 (HMGA2) is a transcriptional modulator that mediates motility and self-renewal in normal and cancer stem cells. We identified increased expression of HMGA2 in the majority of primary human GBM tumors and cell lines compared to normal brain. Additionally, HMGA2 expression was increased in CD133+ GBM neurosphere cells compared to CD133- cells. Targeting HMGA2 with lentiviral short hairpin RNA (shRNA) led to decreased GBM stemness, invasion, and tumorigenicity. Ectopic expression of HMGA2 in GBM cell lines promoted stemness, invasion, and tumorigenicity. Our data suggests that targeting HMGA2 in GBM may be therapeutically beneficial.
胶质母细胞瘤（GBM）包含一群具有干细胞样特性的细胞，这些细胞会促进肿瘤侵袭并导致对治疗产生抗性。识别并靶向GBM中的干细胞因子可能会带来更有效的治疗方法。高迁移率族AT钩蛋白2（HMGA2）是一种转录调节因子，可介导正常干细胞和癌症干细胞的运动性和自我更新能力。我们发现，与正常脑组织相比，大多数原发性人类GBM肿瘤和细胞系中HMGA2的表达均有所增加。此外，与CD133-细胞相比，CD133+ GBM神经球细胞中HMGA2的表达也有所增加。用慢病毒短发夹RNA（shRNA）靶向HMGA2会导致GBM干性、侵袭性和致瘤性降低。在GBM细胞系中异位表达HMGA2会促进干性、侵袭性和致瘤性。我们的数据表明，在GBM中靶向HMGA2可能具有治疗益处。
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