Cancer and meiotic gene expression: Two sides of the same coin?

2区 生物学 Q1 Biochemistry, Genetics and Molecular Biology Current Topics in Developmental Biology Pub Date : 2023-01-01 Epub Date: 2022-07-29 DOI:10.1016/bs.ctdb.2022.06.002
Ieng Fong Sou, Geert Hamer, Wee-Wei Tee, Gerben Vader, Urszula Lucja McClurg
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Abstract

Meiosis increases genetic diversity in offspring by generating genetically unique haploid gametes with reshuffled chromosomes. This process requires a specialized set of meiotic proteins, which facilitate chromosome recombination and segregation. However, re-expression of meiotic proteins in mitosis can have catastrophic oncogenic consequences and aberrant expression of meiotic proteins is a common occurrence in human tumors. Mechanistically, re-activation of meiotic genes in cancer promotes oncogenesis likely because cancers-conversely to healthy mitosis-are fueled by genetic instability which promotes tumor evolution, and evasion of immune response and treatment pressure. In this review, we explore similarities between meiotic and cancer cells with a particular focus on the oncogenic activation of meiotic genes in cancer. We emphasize the role of histones and their modifications, DNA methylation, genome organization, R-loops and the availability of distal enhancers.

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癌症与减数分裂基因表达:一枚硬币的两面?
减数分裂通过产生染色体重新组合的基因独特的单倍体配子来增加后代的遗传多样性。这一过程需要一套专门的减数分裂蛋白,以促进染色体重组和分离。然而,减数分裂蛋白在有丝分裂过程中的重新表达会产生灾难性的致癌后果,减数分裂蛋白的异常表达在人类肿瘤中很常见。从机理上讲,减数分裂基因在癌症中的重新激活会促进肿瘤发生,这可能是因为癌症与健康的有丝分裂相反,其遗传不稳定性会促进肿瘤进化,并逃避免疫反应和治疗压力。在这篇综述中,我们探讨了减数分裂细胞和癌细胞之间的相似之处,尤其关注癌症中减数分裂基因的致癌激活。我们强调组蛋白及其修饰、DNA 甲基化、基因组组织、R 环和远端增强子的作用。
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CiteScore
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发文量
91
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