miR-34a 通过 SIRT1/NFκB 通路参与 Tat 诱导的 HIV-1 长末端重复（LTR）转录激活。
MiR-34a is involved in Tat-induced HIV-1 long terminal repeat (LTR) transactivation through the SIRT1/NFκB pathway.
机构信息
College of Life Science & Bioengineering, Beijing University of Technology, Pingleyuan 100#, District of Chaoyang, Beijing 100124, China.
出版信息
FEBS Lett. 2012 Nov 30;586(23):4203-7. doi: 10.1016/j.febslet.2012.10.023. Epub 2012 Oct 24.
MicroRNAs (miRNAs) regulate gene expression and may contribute to HIV-1 infection. In this study, our goal was to investigate the mechanisms by which miR-34a influenced Tat-induced HIV-1 transactivation through the SIRT1/NFκB pathway. We showed that Tat induced up-regulation of miR-34a expression in TZM-bl cells. MiR-34a significantly inhibited SIRT1 expression. Overexpression of miR-34a increased Tat-induced LTR transactivation. Forced expression of miR-34a decreased SIRT1 protein expression and consequently diminished Tat-induced acetylation of p65, while treatment with a miR-34a inhibitor had the opposite effect. These results suggest that regulating SIRT1 by down-regulation of miR-34a levels may be a therapeutic strategy against HIV-1 replication.
微小 RNA（miRNAs）调节基因表达，可能有助于 HIV-1 感染。在这项研究中，我们的目标是研究 miR-34a 通过 SIRT1/NFκB 通路影响 Tat 诱导的 HIV-1 转录激活的机制。我们表明，Tat 在 TZM-bl 细胞中诱导 miR-34a 表达上调。miR-34a 显著抑制 SIRT1 表达。miR-34a 的过表达增加了 Tat 诱导的 LTR 转录激活。强制表达 miR-34a 降低了 SIRT1 蛋白表达，从而减少了 Tat 诱导的 p65 乙酰化，而 miR-34a 抑制剂的处理则产生相反的效果。这些结果表明，通过下调 miR-34a 水平来调节 SIRT1 可能是一种针对 HIV-1 复制的治疗策略。
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