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首页> 外文期刊>Journal of cellular biochemistry. >Long noncoding RNA opa‐interacting protein 5 antisense transcript 1 promotes proliferation and invasion through elevating integrin α6 expression by sponging miR‐143‐3p in cervical cancer
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Long noncoding RNA opa‐interacting protein 5 antisense transcript 1 promotes proliferation and invasion through elevating integrin α6 expression by sponging miR‐143‐3p in cervical cancer

机译:长度非编码RNA OPA - 相互作用蛋白5反义转录物1通过在宫颈癌中通过冲水-143-3P升高整联蛋白α6表达来促进增殖和侵袭

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摘要

Abstract An increasing number of studies have shown that long noncoding RNAs (lncRNAs) play important roles in cervical cancer (CC) progression. However, the roles and underlying mechanisms of lncRNA opa‐interacting protein 5 antisense transcript 1 (OIP5‐AS1) involved in the CC remain unclear. In the current study, we found that lncRNA OIP5‐AS1 was upregulated in CC tissues and cell lines. High OIP5‐AS1 expression was significantly correlated with advanced International Federation of Gynecology and Obstetrics (FIGO) stage, lymph node metastasis, and poor overall survival of patients with CC. Using in vitro function assays, we showed that OIP5‐AS1 suppression significantly decreased the proliferation, colony formation, and invasion ability of CC cells. Moreover, we revealed that OIP5‐AS1 could act as a competing endogenous RNA of miR‐143‐3p to regulate the ITGA6 expression. Rescue assays showed that miR‐143‐3p inhibitors or ITGA6 overexpression could reverse the inhibitory effects of OIP5‐AS1 suppression on the proliferation and invasion in CC cells. In addition, OIP5‐AS1 suppression reduced tumor growth in vivo. In conclusion, we demonstrated that OIP5‐AS1 promoted proliferation and invasion of CC cells via increasing the ITGA6 expression by sponging miR‐143‐3p, which might be an effective therapeutic target for the treatment of patients with CC.
机译:摘要越来越多的研究表明,长度非编码RNA(LNCRNA)在宫颈癌(CC)进展中起重要作用。然而,在CC中涉及的LNCrNA OPA相互作用蛋白5的角色和潜在机制涉及CC的反义转录物1(OIP5-AS1)仍然尚不清楚。在目前的研究中,我们发现在CC组织和细胞系中上调LNCRNA OIP5-AS1。高OIP5-AS1表达与先进的国际妇科和妇产科(FICO)阶段,淋巴结转移以及CC患者的贫困总体存活率有显着相关。使用体外功能测定,我们表明OIP5-AS1抑制显着降低了CC细胞的增殖,菌落形成和侵袭能力。此外,我们透露,OIP5-AS1可以充当MIR-143-3P的竞争内源RNA,以调节ITGA6表达。抢救测定表明,MiR-143-3P抑制剂或ITGA6过表达可以逆转OIP5-AS1抑制对CC细胞增殖和侵袭的抑制作用。此外,OIP5-AS1抑制减少了体内肿瘤生长。总之,我们证明,OIP5-AS1通过海绵MIR-143-3P增加ITGA6表达来促进CC细胞的增殖和侵袭,这可能是治疗CC患者的有效治疗靶标。

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