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HBP1转录抑制因子与p38丝裂原活化蛋白激酶:G1期调控和肿瘤抑制中的非典型搭档

The HBP1 transcriptional repressor and the p38 MAP kinase: unlikely partners in G1 regulation and tumor suppression.

作者信息

Yee Amy S, Paulson Eric K, McDevitt Michael A, Rieger-Christ Kimberly, Summerhayes Ian, Berasi Stephen P, Kim Jiyoung, Huang Chun-Yin, Zhang Xiaowei

机构信息

Department of Biochemistry, Tufts University School of Medicine, Boston, MA 02111, USA.

出版信息

Gene. 2004 Jul 7;336(1):1-13. doi: 10.1016/j.gene.2004.04.004.

Abstract

Mechanisms that inhibit cell cycle progression and establish growth arrest are fundamental to tumor suppression and to normal cell differentiation. A complete understanding of these mechanisms should provide new diagnostic and therapeutic targets for future clinical applications related to cancer-specific pathways. This review will focus on the HMG-box protein 1 (HBP1) transcriptional repressor and its roles in cell cycle progression and tumor suppression. The work of several labs now suggests a new pathway for inhibiting G1 progression with exciting possible implications for tumor suppression. Our recent work suggests that the two previously unassociated proteins-the HBP1 transcription factor and the p38 MAP kinase pathway-may now participate together in a G1 regulatory network. Several recent papers collectively highlight an unexpected role and connection of the p38 MAP kinase-signaling pathway in cell cycle control, senescence, and tumor suppression. Together, these initially divergent observations may provide clues into a new tumor suppressive network and spur further investigations that may contribute to new diagnostic and therapeutic targets for cancer.

摘要

抑制细胞周期进程并导致生长停滞的机制对于肿瘤抑制和正常细胞分化至关重要。全面了解这些机制应为未来与癌症特异性途径相关的临床应用提供新的诊断和治疗靶点。本综述将聚焦于HMG盒蛋白1(HBP1)转录抑制因子及其在细胞周期进程和肿瘤抑制中的作用。几个实验室的研究现在提示了一条抑制G1期进程的新途径,这对肿瘤抑制可能具有令人兴奋的潜在意义。我们最近的研究表明,两种先前未关联的蛋白——HBP1转录因子和p38丝裂原活化蛋白激酶途径——现在可能共同参与一个G1期调控网络。最近的几篇论文共同强调了p38丝裂原活化蛋白激酶信号通路在细胞周期控制、衰老和肿瘤抑制中出人意料的作用及联系。这些最初看似不同的观察结果共同可能为一个新的肿瘤抑制网络提供线索,并推动进一步的研究,这可能有助于为癌症开发新的诊断和治疗靶点。

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