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Long non‐coding RNA LINC01137 contributes to oral squamous cell carcinoma development and is negatively regulated by miR-22-3p
Cellular Oncology ( IF 6.6 ) Pub Date : 2021-04-02 , DOI: 10.1007/s13402-021-00586-0
Yong Du 1, 2 , Haiyan Yang 3 , Yue Li 2, 4 , Wenli Guo 2 , Yufeng Zhang 5 , Haitao Shen 2 , Lingxiao Xing 2 , Yuehong Li 3 , Wenxin Wu 3 , Xianghong Zhang 2, 3
Affiliation  

Purpose

Long noncoding RNAs (lncRNAs) are emerging as key regulators in cancer initiation and progression. LINC01137 is a recently identified lncRNA of which the functional role in the development of oral squamous cell carcinoma (OSCC) has not been determined yet.

Methods

We analyzed the expression of LINC01137 using a microarray-based OSCC gene expression dataset (GSE31056), and validated the results obtained using RT-qPCR in 26 pairs of primary OSCC tumor tissues and adjacent non-tumor tissues. The proliferative and invasive effects of LINC01137 on OSCC cells were determined using CCK-8, colony formation and transwell assays, respectively. Targeted binding between miR-22-3p and LINC01137 was verified using a dual luciferase reporter assay.

Results

We found that LINC01137 was significantly upregulated in primary OSCCs. LINC01137 knockdown inhibited OSCC cell proliferation, migration and invasion, whereas LINC01137 overexpression induced opposite effects. LINC01137 upregulation along with p53 inhibition enhanced the malignant transformation of oral cells. In addition, we found that miR-22-3p can directly target LINC01137 through interaction with a putative miR-22-3p-binding site present within the LINC01137 sequence. A significant negative correlation was observed between LINC01137 and miR-22-3p expression in primary OSCC specimens. Exogenous overexpression of miR-22-3p markedly reduced the endogenous expression level of LINC01137 in OSCC cells. Additional functional assays showed that miR-22-3p overexpression enhanced the inhibitory effect of siRNA-mediated LINC01137 silencing on OSCC cell proliferation, migration and invasion, whereas miR-22-3p inhibition had the opposite effect.

Conclusions

Our results indicate that LINC01137 functions as an oncogenic lncRNA in OSCC. miR-22-3p can directly target LINC01137 and negatively regulate its expression and function.



中文翻译:

长链非编码 RNA LINC01137 促进口腔鳞状细胞癌的发展,并受 miR-22-3p 的负调控

目的

长链非编码 RNA (lncRNA) 正在成为癌症发生和发展的关键调节因子。LINC01137 是最近发现的 lncRNA,其在口腔鳞状细胞癌 (OSCC) 发展中的功能作用尚未确定。

方法

我们使用基于微阵列的 OSCC 基因表达数据集 (GSE31056) 分析了 LINC01137 的表达,并验证了使用 RT-qPCR 在 26 对原发性 OSCC 肿瘤组织和邻近非肿瘤组织中获得的结果。LINC01137 对 OSCC 细胞的增殖和侵袭作用分别使用 CCK-8、集落形成和 transwell 测定确定。使用双荧光素酶报告基因检测验证了 miR-22-3p 和 LINC01137 之间的靶向结合。

结果

我们发现 LINC01137 在原发性 OSCC 中显着上调。LINC01137 敲低抑制 OSCC 细胞增殖、迁移和侵袭,而 LINC01137 过表达诱导相反的效果。LINC01137 上调和 p53 抑制增强了口腔细胞的恶性转化。此外,我们发现 miR-22-3p 可以通过与存在于​​ LINC01137 序列中的假定 miR-22-3p 结合位点的相互作用直接靶向 LINC01137。在原发性 OSCC 标本中观察到 LINC01137 和 miR-22-3p 表达之间显着负相关。miR-22-3p 的外源性过表达显着降低了 OSCC 细胞中 LINC01137 的内源性表达水平。

结论

我们的结果表明 LINC01137 在 OSCC 中作为致癌 lncRNA 起作用。miR-22-3p 可以直接靶向 LINC01137 并负调控其表达和功能。

更新日期:2021-04-02
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