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首页> 外文期刊>Cell cycle >Long noncoding RNA LINC00657 enhances the malignancy of pancreatic ductal adenocarcinoma by acting as a competing endogenous RNA on microRNA-433 to increase PAK4 expression
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Long noncoding RNA LINC00657 enhances the malignancy of pancreatic ductal adenocarcinoma by acting as a competing endogenous RNA on microRNA-433 to increase PAK4 expression

机译：长度非编码RNA LINC00657通过作为MicroRNA-433上的竞争内源RNA来增强胰腺导管腺癌的恶性肿瘤，以增加PAK4表达

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摘要

A long noncoding RNAs (lncRNA) called LINC00657 is dysregulated and contributes to tumor progression in a number of human cancer types. However, there is limited information on the expression profile and functions of LINC00657 in pancreatic ductal adenocarcinoma (PDAC). The expression profile of LINC00657 in PDAC was estimated by reverse-transcription quantitative polymerase chain reaction (RT-qPCR). The effects of LINC00657 upregulation on PDAC cell proliferation, apoptosis, migration, and invasion in vitro and tumor growth in vivo were explored using CCK-8, flow cytometry, Transwell migration and invasion assays, and a xenograft tumor formation experiment, respectively. The results revealed that LINC00657 was evidently upregulated in the PDAC tumors and cell lines. High LINC00657 expression significantly correlated with the pathological T stage, lymph node metastasis, and shorter overall survival. Functional analysis demonstrated that LINC00657 knockdown inhibited the proliferation, migration, and invasion while promoted the apoptosis of PDAC cells. In addition, LINC00657 knockdown markedly suppressed tumor growth of these cells in vivo. In terms of the mechanism, LINC00657 could directly interact with microRNA-433 (miR-433) and effectively worked as an miR-433 sponge, thus decreasing the competitive binding of miR-433 to PAK4 mRNA and ultimately increasing PAK4 expression. The actions of LINC00657 knockdown on malignant phenotype of PDAC cells were strongly attenuated by miR-433 inhibition and PAK4 restoration. These results indicate that LINC00657 promotes PDAC progression by increasing the output of the miR-433-PAK4 regulatory loop, thus highlighting the importance of the LINC00657-miR-433-PAK4 network in PDAC pathogenesis.
机译：在许多人类癌症类型中，呼吸失去了一种称为LINC00657的长非致rNA（lncrna）并有助于肿瘤进展。然而，有关LINC00657在胰腺导管腺癌（PDAC）中的表达谱和功能的信息有限。通过反转转录定量聚合酶链反应（RT-QPCR）估计PDAC中LINC00657的表达谱。使用CCK-8，流式细胞术，Transwerl迁移和侵袭测定和异种移植肿瘤形成实验，探讨了LINC00657上调对PDAC细胞增殖，细胞凋亡，迁移和侵袭和体内体外肿瘤生长的影响。结果表明，在PDAC肿瘤和细胞系中明显上调了LINC00657。高LINC00657表达与病理T阶段，淋巴结转移和较短的整体存活率显着相关。功能分析表明，LINC00657敲低抑制了促进PDAC细胞凋亡的同时抑制增殖，迁移和侵袭。此外，LINC00657敲低抑制了体内这些细胞的肿瘤生长。就该机制而言，LINC00657可以直接与MicroRNA-433（miR-433）相互作用，并有效地用作miR-433海绵，从而降低miR-433对pak4 mRNA的竞争结合，并最终增加Pak4表达。 LINC00657敲低对PDAC细胞恶性表型的敲低的抑制作用和PAK4恢复强烈衰减。这些结果表明，LINC00657通过增加MIR-433-PAK4调节回路的产出来促进PDAC进展，从而突出了PDAC发病机制中LINC00657-MIR-433-PAK4网络的重要性。

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