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长链非编码RNA HOTAIRM1通过miR-498/WWOX轴抑制肺腺癌细胞的增殖和侵袭。

LncRNA HOTAIRM1 Inhibits the Proliferation and Invasion of Lung Adenocarcinoma Cells via the miR-498/WWOX Axis.

作者信息

Chen Tian-Jun, Gao Fei, Yang Tian, Li Hong, Li Yang, Ren Hui, Chen Ming-Wei

机构信息

Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, People's Republic of China.

Ultrasound Department, Huashan Central Hospital of Xi'an, Xi'an, Shaanxi 710043, People's Republic of China.

出版信息

Cancer Manag Res. 2020 Jun 9;12:4379-4390. doi: 10.2147/CMAR.S244573. eCollection 2020.

DOI:10.2147/CMAR.S244573
PMID:32606933
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7295110/
Abstract

BACKGROUND

Lung adenocarcinoma (ADC) is a major form of lung cancer, which is a main cause of global cancer-related death in male and female patients. LncRNAs are implicated in tumor development. However, the functions and mechanisms of the LncRNA HOTAIRM1 in ADC are not known.

MATERIALS AND METHODS

Here, the downregulated HOTAIRM1 in ADC was selected by TCGA analysis. Subsequently, qRT-PCR, CCK-8, EdU, cell apoptosis, cell cycle and cell invasion assays were utilized for evaluating the roles of HOTAIRM1 in ADC. Finally, we explored the mechanism of HOTAIRM1 in ADC.

RESULTS

HOTAIRM1 expression was considerably decreased in ADC tissues. The knockdown of HOTAIRM1 promoted the cell cycle, growth, and invasion of ADC. Moreover, HOTAIRM1 competitively bound miR-498 to regulate the expression of WWOX.

CONCLUSION

HOTAIRM1 suppressed the proliferation and invasion of ADC cells via the modulation of miR-498/WWOX axis. This finding suggested that it might be clinically valuable as a biomarker for ADC. Furthermore, the findings suggest LncRNA HOTAIRM1 as a candidate therapeutic target in ADC.

摘要

背景

肺腺癌(ADC)是肺癌的主要类型,是全球男性和女性患者癌症相关死亡的主要原因。长链非编码RNA(LncRNAs)与肿瘤发展有关。然而,LncRNA HOTAIRM1在肺腺癌中的功能和机制尚不清楚。

材料与方法

通过TCGA分析筛选出肺腺癌中表达下调的HOTAIRM1。随后,采用qRT-PCR、CCK-8、EdU、细胞凋亡、细胞周期和细胞侵袭实验来评估HOTAIRM1在肺腺癌中的作用。最后,我们探究了HOTAIRM1在肺腺癌中的作用机制。

结果

肺腺癌组织中HOTAIRM1表达显著降低。敲低HOTAIRM1可促进肺腺癌细胞周期、生长及侵袭。此外,HOTAIRM1通过竞争性结合miR-498来调节WWOX表达。

结论

HOTAIRM1通过调控miR-498/WWOX轴抑制肺腺癌细胞的增殖和侵袭。这一发现表明,它作为肺腺癌的生物标志物可能具有临床价值。此外,这些发现提示LncRNA HOTAIRM1可作为肺腺癌的候选治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99fa/7295110/c1d173bef77e/CMAR-12-4379-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99fa/7295110/c8e38e9bd092/CMAR-12-4379-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99fa/7295110/8fa800c35ac6/CMAR-12-4379-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99fa/7295110/2c241f2fbc22/CMAR-12-4379-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99fa/7295110/f840fdeaa08b/CMAR-12-4379-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99fa/7295110/59453f8359b5/CMAR-12-4379-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99fa/7295110/1588648e47cb/CMAR-12-4379-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99fa/7295110/c1d173bef77e/CMAR-12-4379-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99fa/7295110/c8e38e9bd092/CMAR-12-4379-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99fa/7295110/8fa800c35ac6/CMAR-12-4379-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99fa/7295110/2c241f2fbc22/CMAR-12-4379-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99fa/7295110/f840fdeaa08b/CMAR-12-4379-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99fa/7295110/59453f8359b5/CMAR-12-4379-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99fa/7295110/1588648e47cb/CMAR-12-4379-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99fa/7295110/c1d173bef77e/CMAR-12-4379-g0007.jpg

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