Aberrant expression of MAPK1 and MCTS1 in chronic myeloid leukemia (CML).

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

Abstract

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.

MAPK1和MCTS1在慢性髓性白血病(CML)中的异常表达。
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。
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