MAPK1和MCTS1在慢性髓性白血病(CML)中的异常表达。

microPublication biology Pub Date : 2025-09-18 eCollection Date: 2025-01-01 DOI:10.17912/micropub.biology.001681
Leo Kortendick, Corinna Meyer, Stefan Nagel
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引用次数: 0

摘要

基因组扩增可能导致基因表达异常并支持癌症的发展,包括慢性髓性白血病(CML)。在CML细胞系K-562中,我们最近报道了位于22q11染色体位置的TBX1过表达,与CML标志融合基因BCR::ABL1的一部分BCR::ABL1一起局部共扩增。在这里,我们扩展了该研究,通过鉴定基因组扩增和过表达的MAPK1/ERK2在22q11和MCTS1在Xq22。使用药物抑制剂和sirna介导的敲低实验,我们的数据共同揭示了TBX1, MAPK1和MCTS1之间的新调控联系,这可能在耐药中发挥作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Aberrant expression of MAPK1 and MCTS1 in chronic myeloid leukemia (CML).

Genomic amplification may result in aberrant gene expression and support development of cancer, including chronic myeloid leukemia (CML). In CML cell line K-562, we recently reported overexpression of TBX1 located at chromosomal position 22q11, focally co-amplified together with BCR, part of the CML hallmark fusion gene BCR::ABL1. Here, we extended that study, by identifying genomically amplified and overexpressed MAPK1/ERK2 at 22q11 together with MCTS1 at Xq22. Using pharmacological inhibitors and siRNA-mediated knockdown assays, our data collectively revealed novel regulatory connections between TBX1, MAPK1 and MCTS1, which may play a role in drug resistance.

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