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首页> 外文期刊>Journal of cellular biochemistry. >All‐Trans‐Retinoic Acid Stimulates Overexpression of Tumor Protein D52 (TPD52, Isoform 3) and Neuronal Differentiation of IMR‐32 Cells
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All‐Trans‐Retinoic Acid Stimulates Overexpression of Tumor Protein D52 (TPD52, Isoform 3) and Neuronal Differentiation of IMR‐32 Cells

机译：全反转甲酸刺激肿瘤蛋白D52（TPD52，同种型3）的过表达和IMR-32细胞的神经元分化

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ABSTRACT Tumor protein D52 (TPD52), a proto‐oncogene is overexpressed in a variety of epithelial carcinomas and plays an important role in cell proliferation, migration, and cell death. In the present study we found that the treatment of IMR‐32 neuroblastoma (NB) cells with retinoic acid (RA) stimulates an increase in expression of TPD52. TPD52 expression is detectable after 72?h, can be maintained till differentiation of NB cells suggesting that TPD52 is involved in differentiation. Here, we demonstrate that TPD52 is essential for RA to promote differentiation of NB cells. Our results show that exogenous expression of EGFP‐TPD52 in IMR‐32 cells resulted cell differentiation even without RA. RA by itself and with overexpression of TPD52 can increase the ability of NB cells differentiation. Interestingly, transfection of IMR‐32 cells with a specific small hairpin RNA for efficient knockdown of TPD52 attenuated RA induced NB cells differentiation. Transcriptional and translational level expression of neurotropic (BDNF, NGF, Nestin) and differentiation (β III tubulin, NSE, TH) factors in NB cells with altered TPD52 expression and/or RA treatment confirmed essential function of TPD52 in cellular differentiation. Furthermore, we show that TPD52 protects cells from apoptosis and arrest cell proliferation by varying expression of p27Kip1, activation of Akt and ERK1/2 thus promoting cell differentiation. Additionally, inhibition of STAT3 activation by its specific inhibitor arrested NB cells differentiation by EGFP‐TPD52 overexpression with or without RA. Taken together, our data reveal that TPD52 act through activation of JAK/STAT signaling pathway to undertake NB cells differentiation induced by RA. J. Cell. Biochem. 118: 4358–4369, 2017. ? 2017 Wiley Periodicals, Inc.
机译：摘要肿瘤蛋白D52（TPD52），一种原癌基因在各种上皮癌中过表达，并在细胞增殖，迁移和细胞死亡中起重要作用。在本研究中，我们发现用视黄酸（Ra）的IMR-32神经母细胞瘤（Nb）细胞刺激TPD52表达的增加。在72℃后可以检测到TPD52表达，可以保持直到Nb细胞的分化，表明TPD52参与分化。在这里，我们证明TPD52对于促进Nb细胞的分化是必需的。我们的结果表明，即使没有Ra，IMR-32细胞中EGFP-TPD52的外源表达也会导致细胞分化。 ra本身和TPD52的过表达可以增加Nb细胞分化的能力。有趣的是，用特定小型发夹RNA转染IMR-32细胞，用于有效敲击TPD52减毒RA诱导的Nb细胞分化。具有改变的TPD52表达和/或RA治疗的Nb细胞中Nb细胞中Nb细胞中的神经刺激（BDNF，NGF，巢蛋白，NESE，NSE，TH）因子的转录和翻译水平表达和/或RA处理证实了TPD52在细胞分化中的基本函数。此外，我们表明TPD52通过改变P27KIP1的表达，AKT和ERK1 / 2的激活来保护细胞免受细胞凋亡和抑制细胞增殖，从而促进细胞分化。另外，通过其特异性抑制剂阻止STAT3活化的抑制Nb细胞通过EGFP-TPD52过表达，其具有或不含Ra的抑制。一起使用，我们的数据显示TPD52通过激活JAK /统计信号通路的激活来进行RA诱导的Nb细胞分化。 J.Cell。生物学习。 118：4358-4369,2017。？ 2017年Wiley期刊，Inc。

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