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LMCD1-AS1/miR-526b-3p/OSBPL5 轴促进非小细胞肺癌细胞的增殖、迁移和侵袭。

The LMCD1-AS1/miR-526b-3p/OSBPL5 axis promotes cell proliferation, migration and invasion in non-small cell lung cancer.

机构信息

Department of Thoracic Surgery, Shengli Oilfield Central Hospital, 31 Jinan Road, Dongying, 257034, Shandong, China.

出版信息

BMC Pulm Med. 2022 Jan 9;22(1):30. doi: 10.1186/s12890-022-01820-7.

DOI:10.1186/s12890-022-01820-7
PMID:35000595
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8744214/
Abstract

PURPOSE

To explore the specific role and regulatory mechanism of oxysterol binding protein like 5 (OSBPL5) in non-small cell lung cancer (NSCLC).

METHODS AND RESULTS

Quantitative real-time polymerase chain reaction (qRT-PCR) analysis demonstrated that OSBPL5 expression was notably elevated in NSCLC tissues and cell lines, and Kaplan-Meier analysis manifested that high OSBPL5 expression was closely related to the poor prognosis of NSCLC patients. Besides, according to the results from western blot analysis, cell counting kit-8, EdU and Transwell assays, knockdown of OSBPL5 suppressed NSCLC cell proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) process. Additionally, by performing qRT-PCR analysis, luciferase reporter and RNA pull-down assays, we verified that OSBPL5 was a downstream target of miR-526b-3p and long noncoding RNA (lncRNA) LMCD1-AS1 served as a sponge for miR-526b-3p. Moreover, from rescue assays, we observed that OSBPL5 overexpression offset LMCD1-AS1 knockdown-mediated inhibition in cell proliferation, migration, invasion and EMT in NSCLC.

CONCLUSIONS

This paper was the first to probe the molecular regulatory mechanism of OSBPL5 involving the LMCD1-AS1/miR-526b-3p axis in NSCLC and our results revealed that the LMCD1-AS1/miR-526b-3p/OSBPL5 axis facilitates NSCLC cell proliferation, migration, invasion and EMT, which may offer a novel therapeutic direction for NSCLC.

摘要

目的

探索氧化固醇结合蛋白样 5(OSBPL5)在非小细胞肺癌(NSCLC)中的具体作用和调控机制。

方法和结果

定量实时聚合酶链反应(qRT-PCR)分析表明,OSBPL5 在 NSCLC 组织和细胞系中表达明显上调,Kaplan-Meier 分析表明高 OSBPL5 表达与 NSCLC 患者的不良预后密切相关。此外,根据 Western blot 分析、细胞计数试剂盒-8(CCK-8)、EdU 和 Transwell 检测的结果,敲低 OSBPL5 抑制了 NSCLC 细胞的增殖、迁移、侵袭和上皮-间充质转化(EMT)过程。此外,通过 qRT-PCR 分析、荧光素酶报告基因和 RNA 下拉实验,我们验证了 OSBPL5 是 miR-526b-3p 的下游靶基因,长链非编码 RNA(lncRNA)LMCD1-AS1 作为 miR-526b-3p 的海绵。此外,从挽救实验中,我们观察到 OSBPL5 的过表达抵消了 LMCD1-AS1 敲低介导的 NSCLC 细胞增殖、迁移、侵袭和 EMT 抑制。

结论

本文首次探讨了 OSBPL5 涉及 NSCLC 中 LMCD1-AS1/miR-526b-3p 轴的分子调控机制,我们的结果表明,LMCD1-AS1/miR-526b-3p/OSBPL5 轴促进 NSCLC 细胞的增殖、迁移、侵袭和 EMT,这可能为 NSCLC 提供新的治疗方向。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d1b/8744214/701cc018df48/12890_2022_1820_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d1b/8744214/be6bd49c3003/12890_2022_1820_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d1b/8744214/977d82ad5f32/12890_2022_1820_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d1b/8744214/31df43f3c024/12890_2022_1820_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d1b/8744214/a580ac6d7288/12890_2022_1820_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d1b/8744214/701cc018df48/12890_2022_1820_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d1b/8744214/be6bd49c3003/12890_2022_1820_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d1b/8744214/977d82ad5f32/12890_2022_1820_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d1b/8744214/31df43f3c024/12890_2022_1820_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d1b/8744214/a580ac6d7288/12890_2022_1820_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d1b/8744214/701cc018df48/12890_2022_1820_Fig5_HTML.jpg

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