Retinal Biology Research Laboratory, Veterans Administration Medical Center, Kansas City, Missouri, United States of America ; Department of Neurology, Kansas University Medical Center, Kansas City, Kansas, United States of America.
PLoS One. 2013 Sep 11;8(9):e73786. doi: 10.1371/journal.pone.0073786. eCollection 2013.
γ-Synuclein is a member of the synucleins family of small proteins, which consists of three members:α, β- and γ-synuclein. γ-Synuclein is abnormally expressed in a high percentage of advanced and metastatic tumors, but not in normal or benign tissues. Furthermore, γ-synuclein expression is strongly correlated with disease progression, and can stimulate proliferation, induce invasion and metastasis of cancer cells. γ-Synuclein transcription is regulated basically through the binding of AP-1 to specific sequences in intron 1. Here we show that γ-synuclein expression may be also regulated by micro RNAs (miRs) on post-transcriptional level. According to prediction by several methods, the 3'-untranslated region (UTR) of γ-synuclein gene contains targets for miRs. Insertion of γ-synuclein 3'-UTR downstream of the reporter luciferase (LUC) gene causes a 51% reduction of LUC activity after transfection into SKBR3 and Y79 cells, confirming the presence of efficient targets for miRs in this fragment. Expression of miR-4437 and miR-4674 for which putative targets in 3'-UTR were predicted caused a 61.2% and 60.1% reduction of endogenous γ-synuclein expression confirming their role in gene expression regulation. On the other hand, in cells overexpressing γ-synuclein no significant effect of miRs on γ-synuclein expression was found suggesting that miRs exert their regulatory effect only at low or moderate, but not at high level of γ-synuclein expression. Elevated level of γ-synuclein differentially changes the level of several miRs expression, upregulating the level of some miRs and downregulating the level of others. Three miRs upregulated as a result of γ-synuclein overexpression, i.e., miR-885-3p, miR-138 and miR-497 have putative targets in 3'-UTR of the γ-synuclein gene. Some of miRs differentially regulated by γ-synuclein may modulate signaling pathways and cancer related gene expression. This study demonstrates that miRs might provide cell-specific regulation of γ-synuclein expression and set the stage to further evaluate their role in pathophysiological processes.
γ-突触核蛋白是小蛋白家族突触核蛋白的一个成员,由三个成员组成:α、β-和γ-突触核蛋白。γ-突触核蛋白在高比例的晚期和转移性肿瘤中异常表达,但不在正常或良性组织中表达。此外,γ-突触核蛋白的表达与疾病的进展密切相关,并能刺激癌细胞的增殖、诱导其侵袭和转移。γ-突触核蛋白的转录基本通过 AP-1 与内含子 1 中的特定序列结合来调节。在这里,我们表明 γ-突触核蛋白的表达也可能受到转录后水平 microRNAs(miRs)的调节。根据几种方法的预测,γ-突触核蛋白基因的 3'-非翻译区(UTR)包含 miRs 的靶标。将 γ-突触核蛋白 3'-UTR 插入报告荧光素酶(LUC)基因的下游,导致转染 SKBR3 和 Y79 细胞后 LUC 活性降低 51%,证实该片段中存在有效的 miR 靶标。预测 3'-UTR 中有靶标的 miR-4437 和 miR-4674 的表达导致内源性 γ-突触核蛋白表达降低 61.2%和 60.1%,证实了它们在基因表达调控中的作用。另一方面,在过表达 γ-突触核蛋白的细胞中,miRs 对 γ-突触核蛋白表达没有显著影响,这表明 miRs 仅在 γ-突触核蛋白表达的低或中等水平,而不是在高表达水平发挥其调节作用。γ-突触核蛋白水平的升高会导致几种 miRs 表达水平的差异变化,上调某些 miRs 的表达水平,下调其他 miRs 的表达水平。由于 γ-突触核蛋白过表达而上调的三个 miR,即 miR-885-3p、miR-138 和 miR-497,在 γ-突触核蛋白基因的 3'-UTR 中有靶标。一些由 γ-突触核蛋白差异调节的 miRs 可能调节信号通路和癌症相关基因的表达。本研究表明,miRs 可能为 γ-突触核蛋白表达提供细胞特异性调节,并为进一步评估其在生理病理过程中的作用奠定了基础。