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首页> 美国卫生研究院文献>Journal of Cellular and Molecular Medicine >PCAT‐1 promotes cell growth by sponging miR‐129 via MAP3K7/NF‐κB pathway in multiple myeloma
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PCAT‐1 promotes cell growth by sponging miR‐129 via MAP3K7/NF‐κB pathway in multiple myeloma

机译：PCAT-1通过多发性骨髓瘤中的MAP3K7 /NF-κB途径使miR-129海绵化从而促进细胞生长

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摘要

Loss of one or some specific miRNA‐mediated regulation is closely associated with malignant progression of multiple myeloma (MM). But how these miRNAs work and what role the specific miRNA plays in this process of malignant progression remain unclear. It was found in this study that the expression of miR‐129 was decreased in both MM cell lines and newly diagnosed MM patients. Further clinicopathological statistics showed that miR‐129 was correlated with the isotype of MM patients. MiR‐129 overexpression disturbed cell proliferation, cell cycle evolution and spurred apoptosis both in vitro and in vivo. MAP3K7, a kinase able to activate NF‐κB circuit, was found to be up‐regulated in MM and contain a binding target of miR‐129. In addition, lncRNA PCAT‐1 functioned to sponge miR‐129 and thereby lowered its expression. PCAT‐1 knockdown eliminated the tumour‐promoting effect caused by miR‐129 inhibition, probably through repressing MAP3K7 and subsequent NF‐κB activation. To the best of our knowledge, this is the first study to have discovered that increased expression of PCAT‐1 could augment cell proliferation and cycle procession and inhibit apoptosis by down‐regulating miR‐129 via the MAP3K7/NF‐κB pathway in MM.
机译：一种或某些特定的miRNA介导的调节丧失与多发性骨髓瘤（MM）的恶性进展密切相关。但是，这些miRNA如何发挥作用以及特定的miRNA在恶性进展过程中起什么作用仍不清楚。在这项研究中发现，在MM细胞系和新诊断的MM患者中，miR-129的表达均降低。进一步的临床病理统计表明，miR-129与MM患者的同种型相关。 MiR-129的过表达在体外和体内扰乱细胞增殖，细胞周期进化并刺激细胞凋亡。能够激活NF-κB回路的激酶MAP3K7在MM中被上调，并含有miR-129的结合靶标。另外，lncRNA PCAT-1发挥海绵miR-129的作用，从而降低了其表达。 PCAT-1敲除消除了由miR-129抑制引起的促肿瘤作用，可能是通过抑制MAP3K7和随后的NF-κB激活。据我们所知，这是第一项发现PCAT-1表达增加可通过MM中经由MAP3K7 /NF-κB通路下调miR-129来增强细胞增殖和周期进程并抑制细胞凋亡的研究。

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