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转化刺激克隆22(TSC-22)与含溴结构域蛋白7(BRD7)直接相互作用,以增强对卵巢癌中细胞外信号调节激酶(ERK)通路的抑制作用。

Transforming Stimulated Clone 22 (TSC-22) Interacts Directly with Bromodomain-Containing Protein 7 (BRD7) to Enhance the Inhibition of Extracellular Signal-Regulate Kinase (ERK) Pathway in Ovarian Cancer.

作者信息

Lee Seung-Hoon, Choi Donchan

机构信息

Department of Life Science, YongIn University, Yongin 17092, Korea.

出版信息

Dev Reprod. 2022 Sep;26(3):117-126. doi: 10.12717/DR.2022.26.3.117. Epub 2022 Sep 30.

Abstract

Bromodomain-containing protein 7 (BRD7) participates in many cellular processes and embryo development. BRD7 is down-regulated in various cancers and evidence of its tumor suppressor function has been accumulating. Here, we identified transforming stimulated clone 22 (TSC-22) as a novel BRD7 interacting protein and show its novel function as a positive regulator of BRD7. We found that TSC-22 expression potentiated the inactivation of the extracellular signal-regulate kinase (ERK) pathway by BRD7. Our data establishes TSC-22 as a modulator of BRD7 and unravels the molecular mechanisms that drive the synergistic tumor-suppressing effects of TSC-22 and BRD7. Our findings may open new avenues for developing novel molecular therapies for tumors exhibiting down-regulated BRD7 and/or TSC-22.

摘要

含溴结构域蛋白7(BRD7)参与许多细胞过程和胚胎发育。BRD7在多种癌症中表达下调,其肿瘤抑制功能的证据也在不断积累。在此,我们鉴定出转化刺激克隆22(TSC-22)是一种新型的与BRD7相互作用的蛋白,并展示了其作为BRD7正向调节因子的新功能。我们发现TSC-22的表达增强了BRD7对细胞外信号调节激酶(ERK)途径的失活作用。我们的数据确定TSC-22为BRD7的调节剂,并揭示了驱动TSC-22和BRD7协同肿瘤抑制作用的分子机制。我们的发现可能为开发针对BRD7和/或TSC-22表达下调的肿瘤的新型分子疗法开辟新途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/383d/9578317/964587443d97/dr-26-3-117-g1.jpg

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