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环状CCT3通过miR-107/ Wnt/ FGF7轴增强非小细胞肺癌（NSCLC）的侵袭和上皮-间质转化（EMT）

circCCT3 Enhances Invasion and Epithelial-Mesenchymal Transition (EMT) of Non-Small-Cell Lung Cancer (NSCLC) via the miR-107/Wnt/FGF7 Axis.

作者信息

Li Jinyou, Lu Rongguo, Yang Kejia, Sun Qi

机构信息

Department of Thoracic Surgery, Affiliated Hospital of Jiangnan University, Wuxi, China.

Department of Thoracic Surgery, Wuxi People's Hospital, Wuxi, China.

出版信息

J Oncol. 2022 Jun 22;2022:7020774. doi: 10.1155/2022/7020774. eCollection 2022.

DOI:10.1155/2022/7020774
PMID:35783154
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9242791/
Abstract

BACKGROUND

CircRNAs play a role in a variety of biological processes, including tumorigenesis. circCCT3 has been shown to regulate cancer initiation and progression. Unfortunately, whether circCCT3 is involved in non-small-cell lung cancer (NSCLC) metastasis remains unclear.

METHODS

Our study utilized RT-qPCR to examine gene expression levels. A transwell assay was used to measure invasion ability of cells. Starbase software and TargetScan software were used to predict target genes.

RESULTS

circCCT3 knockdown attenuated invasion and epithelial-mesenchymal transition (EMT) of A549 and Calu-1 cells. miR-107 mimics could rescue circCCT3-induced invasion and EMT. Next, miR-107 mimics and circCCT3 knockdown suppressed Wnt3a and FGF7 expression. An miR-107 inhibitor promoted Wnt3a and FGF7 expressions. Finally, FGF7 greatly restored miR-107-inhibited invasion and EMT of A549 cells.

CONCLUSION

Here, we reveal a molecular mechanism circCCT3/miR-107/Wnt/FGF7 responsible for NSCLC metastasis.

摘要

背景

环状RNA（circRNAs）在包括肿瘤发生在内的多种生物学过程中发挥作用。circCCT3已被证明可调节癌症的起始和进展。遗憾的是，circCCT3是否参与非小细胞肺癌（NSCLC）转移仍不清楚。

方法

我们的研究利用逆转录定量聚合酶链反应（RT-qPCR）检测基因表达水平。采用Transwell实验检测细胞的侵袭能力。使用Starbase软件和TargetScan软件预测靶基因。

结果

circCCT3敲低减弱了A549和Calu-1细胞的侵袭及上皮-间质转化（EMT）。miR-107模拟物可挽救circCCT3诱导的侵袭和EMT。接下来，miR-107模拟物和circCCT3敲低抑制了Wnt3a和FGF7的表达。miR-107抑制剂促进了Wnt3a和FGF7的表达。最后，FGF7极大地恢复了miR-107抑制的A549细胞的侵袭和EMT。

结论

在此，我们揭示了一种负责NSCLC转移的circCCT3/miR-107/Wnt/FGF7分子机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61a1/9242791/2a022bdb7863/JO2022-7020774.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61a1/9242791/d697d2320cf6/JO2022-7020774.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61a1/9242791/ec535c035432/JO2022-7020774.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61a1/9242791/f77cc2075be9/JO2022-7020774.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61a1/9242791/2a022bdb7863/JO2022-7020774.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61a1/9242791/d697d2320cf6/JO2022-7020774.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61a1/9242791/ec535c035432/JO2022-7020774.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61a1/9242791/f77cc2075be9/JO2022-7020774.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/61a1/9242791/2a022bdb7863/JO2022-7020774.004.jpg

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