CD320在乳腺癌干细胞中的表达增加,但不促进其扩增或改变关键组蛋白甲基化标记。

microPublication biology Pub Date : 2025-09-04 eCollection Date: 2025-01-01 DOI:10.17912/micropub.biology.001696
Christine Carney, Lisa Jenkins, Connor Jewell, Rachel Carter, Puneet Mann, Binwu Tang, Senthil Muthuswamy, Lalage Wakefield
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引用次数: 0

摘要

一些证据表明,茎干性与维生素B12之间存在潜在联系,维生素B12有助于s -腺苷蛋氨酸(SAM)的产生,从而促进甲基化依赖性表观遗传控制。在这里,我们发现维生素B12受体CD320在三阴性乳腺癌模型的癌症干细胞(CSCs)中显著增加。我们假设CD320表达的升高通过增加sam介导的组蛋白H3K4和H3K36三甲基化来促进CSC扩张性自我更新,这在之前与干细胞和可塑性有关。然而,我们发现CD320表达的调节对SAM、H3K4me3和H3K36me3水平没有影响,也没有影响体外CSC的扩增。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

CD320 expression is increased in breast cancer stem cells but does not promote their expansion or alter key histone methylation marks.

CD320 expression is increased in breast cancer stem cells but does not promote their expansion or alter key histone methylation marks.

Several lines of evidence suggest a potential link between stemness and vitamin B12, which contributes to S-adenosylmethionine (SAM) generation and hence methylation-dependent epigenetic control. Here we found that the vitamin B12 receptor, CD320, is significantly increased in cancer stem cells (CSCs) in models of triple-negative breast cancer . We hypothesized that elevated CD320 expression promotes CSC expansive self-renewal via increased SAM-mediated histone H3K4 and H3K36 trimethylation, which were previously implicated in stemness and plasticity. However, we found that modulation of CD320 expression had no effect on SAM, H3K4me3 and H3K36me3 levels, or on CSC expansion in vitro .

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