Knowles Truman, Huang Tina, Qi Jin, An Shejuan, Burket Noah, Cooper Scott, Nazarian Javad, Saratsis Amanda M
W.M. Keck Science Department, Scripps, Pitzer, and Claremont McKenna Colleges, Claremont, CA 91711, USA.
Department of Neurosurgery, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.
Cancers (Basel). 2023 Jun 19;15(12):3241. doi: 10.3390/cancers15123241.
Diffuse midline glioma (DMG) is the most lethal of all childhood cancers. DMGs are driven by histone-tail-mutation-mediated epigenetic dysregulation and partner mutations in genes controlling proliferation and migration. One result of this epigenetic and genetic landscape is the overexpression of LIN28B RNA binding protein. In other systems, LIN28B has been shown to prevent let-7 microRNA biogenesis; however, let-7, when available, faithfully suppresses tumorigenic pathways and induces cellular maturation by preventing the translation of numerous oncogenes. Here, we review the current literature on LIN28A/B and the let-7 family and describe their role in gliomagenesis. Future research is then recommended, with a focus on the mechanisms of LIN28B overexpression and localization in DMG.
弥漫性中线胶质瘤（DMG）是所有儿童癌症中致死率最高的。DMG由组蛋白尾部突变介导的表观遗传失调以及控制增殖和迁移的基因中的伙伴突变驱动。这种表观遗传和基因格局的一个结果是LIN28B RNA结合蛋白的过表达。在其他系统中，LIN28B已被证明可阻止let-7微小RNA的生物合成；然而，let-7在可用时，通过阻止众多癌基因的翻译，忠实地抑制致癌途径并诱导细胞成熟。在这里，我们综述了关于LIN28A/B和let-7家族的当前文献，并描述了它们在胶质瘤发生中的作用。然后建议进行未来研究，重点是LIN28B在DMG中的过表达和定位机制。
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