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首页> 外文期刊>Cell biology international. >Down-regulation of lncRNA OGFRP1 induces autophagy and growth inhibition by AKT/mTOR signaling pathway in HCAECs
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Down-regulation of lncRNA OGFRP1 induces autophagy and growth inhibition by AKT/mTOR signaling pathway in HCAECs

机译：LNCRNA OGFRP1的下调诱导HCAEC中AKT / MTOR信号传导途径的自噬和生长抑制

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摘要

Long noncoding RNAs (lncRNAs) have been found to play important roles in nearly all biological processes. However, the functions of the majority of LncRNAs are not fully clear. Here we evaluated the function of lncRNA OGFRP1, which has not been previously annotated, in human coronary artery endothelial cells (HCAECs). First, we knocked down lncRNA OGFRP1 in HCAECs by using siRNA transfection. qRT-PCR results indicated that siRNA1 and siRNA3 both had potent interference efficiencies. Next, by using CCK8 assay and clone formation assay, we found that siRNA3 transfection induced growth inhibition in HCAECs. Cell migration and invasion were also found to be inhibited in OGFRP1 silenced cells. Moreover, siRNA1 transfection further verified the inhibitory effects of lncRNA OGFRP1 knockdown on the proliferation, migration and invasion of HCAECs. Flow cytometry detection demonstrated that OGFRP1 knockdown induced cell cycle arrest and apoptosis. Western blot assay indicated that p70S6K and CyclinD1 were down-regulated by knockdown of OGFRP1. The intrinsic apoptosis pathway was activated in lncRNA OGFRP1 silenced cells, including increased Bax and Active-caspase 3 and decreased Bcl2. The expression of autophagy markers LC3 and Beclin1 was increased and p62 decreased, all of which indicated that cell autophagy was promoted by down-regulation of lncRNA OGFRP1. Mechanistic studies showed that lncRNA OGFRP1 inhibited the AKT/mTOR signaling pathway, including increasing phosphorylation level of AKT, mTOR and GSK3 beta. In conclusion, we find that down-regulation of lncRNA induces autophagy and inhibited the proliferation, migration and invasion by AKT/mTOR signaling pathway in HCAECs.
机译：已经发现长期非编码RNA（LNCRNA）在几乎所有生物过程中发挥重要作用。但是，大多数LNCRNA的功能并不完全清楚。在这里，我们评估了LNCRNA OGFRP1的功能，该功能在人冠状动脉内皮细胞（HCAEC）中尚未注释。首先，通过使用siRNA转染在HCAEC中击倒LNCRNA OGFRP1。 QRT-PCR结果表明siRNA1和siRNA3都具有强烈的干扰效率。接下来，通过使用CCK8测定和克隆形成测定，我们发现siRNA3转染诱导HCAEC中的生长抑制。还发现细胞迁移和侵袭在OGFRP1沉默的细胞中受到抑制。此外，siRNA1转染进一步验证了LNCRNA OGFRP1敲低对HCAECS增殖，迁移和侵袭的抑制作用。流式细胞术检测证明OGFRP1敲低诱导细胞周期停滞和细胞凋亡。 Western印迹测定表明P70S6K和CyclinD1通过OGFRP1的敲低来调节。内在凋亡途径在LNCRNA OGFRP1沉默的细胞中激活，包括增加的BAX和活性胱天冬酶3并降低BCL2。自噬标志物LC3和BEC11的表达增加，P62降低，所有这些都表明通过LNCRNA OGFRP1的下调促进细胞自噬。机械研究表明，LNCRNA OGFRP1抑制AKT / mTOR信号传导途径，包括增加AKT，MTOR和GSK3β的磷酸化水平。总之，我们发现LNCRNA的下调诱导自噬并抑制HCAEC中AKT / MTOR信号传导途径的增殖，迁移和侵袭。

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