Polyadenylation of canonical histone H3.1 in carcinogenesis.
Polyadenylation of canonical histone H3.1 in carcinogenesis.
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DOI：
10.1016/bs.apha.2022.08.003
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发表时间：
2023
期刊：
影响因子：
--
通讯作者：
Costa M
中科院分区：
文献类型：
--
作者：
Veerappan A;Stavrou A;Costa M
典型的组蛋白信使RNA（mRNA）在S期转录，并且在3′端不以poly（A）尾终止。相反，组蛋白mRNA在其3-末端显示茎环结构。茎环结合蛋白（SLBP）结合茎环并调节典型组蛋白mRNA代谢。我们以前证明，暴露于砷，环境致癌物，诱导典型的组蛋白H3.1 mRNA的聚腺苷酸化，导致体外人类细胞的转化。砷通过表观遗传机制诱导蛋白酶体降解和抑制SLBP转录，从而降低SLBP的细胞水平。同样，我们还报道了镍和砷对典型组蛋白mRNA转录和翻译的影响相似。最近，我们进一步证明双酚的暴露增加了典型组蛋白H3.1 mRNA的聚腺苷酸化，可能是通过下调SLBP表达。这促进了至少一种典型组蛋白同种型（H3.1）的异常稳定性，并且还增加了H3蛋白水平。经典组蛋白的过量表达已显示出增加对DNA损伤的敏感性以及增加缺失染色体的频率并诱导基因组不稳定性。因此，多聚腺苷酸化的典型组蛋白mRNA砷，镍和双酚暴露可能有助于金属和双酚诱导的致癌作用。
Canonical histone messenger RNAs (mRNAs) are transcribed during S phase and do not terminate with a poly(A) tail at the 3′ end. Instead, the histone mRNAs display a stem-loop structure at their 3-end. Stem-loop-binding protein (SLBP) binds the stem-loop and regulates canonical histone mRNA metabolism. We previously demonstrated that exposure to arsenic, an environmental carcinogen, induces polyadenylation of canonical histone H3.1 mRNA, causing transformation of human cells in vitro. Arsenic decreased cellular levels of SLBP by inducing its proteasomal degradation and inhibiting SLBP transcription via epigenetic mechanisms. Similarly, we also reported that nickel and arsenic have similar effects on canonical histone mRNA transcription and translation. Most recently, we further demonstrated that bisphenols’ exposure increased polyadenylation of canonical histone H3.1 mRNA possibly through down-regulation of SLBP expression. This facilitates the abnormal stability of at least one canonical histone isoform (H3.1), and also increases H3 protein levels. Excess expression of canonical histones have been shown to increase sensitivity to DNA damage as well as increase the frequency of missing chromosomes and induce genomic instability. Thus, polyadenylation of canonical histone mRNA following arsenic, nickel and bisphenols exposure may contribute to metal and bisphenol-induced carcinogenesis.
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影响因子：
64.5
作者：
Goldberg AD;Banaszynski LA;Noh KM;Lewis PW;Elsaesser SJ;Stadler S;Dewell S;Law M;Guo X;Li X;Wen D;Chapgier A;DeKelver RC;Miller JC;Lee YL;Boydston EA;Holmes MC;Gregory PD;Greally JM;Rafii S;Yang C;Scambler PJ;Garrick D;Gibbons RJ;Higgs DR;Cristea IM;Urnov FD;Zheng D;Allis CD
通讯作者：
Allis CD
影响因子：
10.5
作者：
Sullivan, E;Santiago, C;Duronio, RJ
通讯作者：
Duronio, RJ
影响因子：
3.7
作者：
Jordan A;Zhang X;Li J;Laulicht-Glick F;Sun H;Costa M
通讯作者：
Costa M
影响因子：
3.9
作者：
Bush KM;Yuen BT;Barrilleaux BL;Riggs JW;O'Geen H;Cotterman RF;Knoepfler PS
通讯作者：
Knoepfler PS
影响因子：
5.3
作者：
HARRIS, ME;BOHNI, R;MARZLUFF, WF
通讯作者：
MARZLUFF, WF