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神经生长因子 4/叉头框蛋白 L1 在非小细胞肺癌发展中的作用。

The Role of Neurotrophin-4/Forkhead Box L1 in the Development of Nonsmall-Cell Lung Cancer.

机构信息

Department of Pulmonary and Critical Care Medicine, Heping Hospital Affiliated to Changzhi Medical College, Changzhi, China.

Department of General Surgery, PLA Rocket Force Characteristic Medical Center, Beijing, China.

出版信息

Contrast Media Mol Imaging. 2022 Aug 9;2022:9078012. doi: 10.1155/2022/9078012. eCollection 2022.

DOI:10.1155/2022/9078012
PMID:36034210
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9381233/
Abstract

This study aims to uncover the biological function of neurotrophin-4 (NTF4) in affecting the progression of nonsmall-cell lung cancer (NSCLC). NTF4 levels in NSCLC and paracancerous tissues were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Knockdown of NTF4 in A549 and H1299 cells was achieved by transfection of sh-NTF4. Subsequently, proliferative and migratory changes in NSCLC cells with NTF4 knockdown were determined by cell counting kit-8 (CCK-8) and transwell and wound healing assay. The target gene binding NTF4 was predicted by bioinformatic software and verified by a dual-luciferase reporter assay. The role of the NTF4/FOXL1 axis in mediating NSCLC cell behaviors was finally explored through rescue experiments. NTF4 was highly expressed in NSCLC tissues than in normal ones. Knockdown of NTF4 remarkably reduced proliferative and migratory rates in A549 and H1299 cells. Forkhead Box L1 (FOXL1) was confirmed as a target gene of NTF4 by bioinformatic software and verified by a dual-luciferase reporter assay. Knockdown of FOXL1 was able to reverse the reduced proliferative and migratory rates in A549 and H1299 cells transfected with sh-NTF4. NTF4 triggers NSCLC to proliferate and migrate via negatively regulating FOXL1.

摘要

本研究旨在揭示神经营养因子-4（NTF4）在影响非小细胞肺癌（NSCLC）进展中的生物学功能。通过实时定量聚合酶链反应（qRT-PCR）检测 NSCLC 和癌旁组织中的 NTF4 水平。通过 sh-NTF4 转染敲低 A549 和 H1299 细胞中的 NTF4。随后，通过细胞计数试剂盒-8（CCK-8）和 Transwell 及划痕愈合实验测定 NTF4 敲低后 NSCLC 细胞的增殖和迁移变化。生物信息学软件预测 NTF4 的靶基因，并通过双荧光素酶报告基因实验验证。最后，通过挽救实验探讨 NTF4/FOXL1 轴在介导 NSCLC 细胞行为中的作用。NTF4 在 NSCLC 组织中表达高于正常组织。敲低 NTF4 可显著降低 A549 和 H1299 细胞的增殖和迁移率。叉头框 L1（FOXL1）被生物信息学软件确认为 NTF4 的靶基因，并通过双荧光素酶报告基因实验验证。敲低 FOXL1 可逆转转染 sh-NTF4 的 A549 和 H1299 细胞中增殖和迁移率降低的情况。NTF4 通过负调控 FOXL1 触发 NSCLC 增殖和迁移。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1586/9381233/ee0daa2323b6/CMMI2022-9078012.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1586/9381233/2838af7294bc/CMMI2022-9078012.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1586/9381233/c371165d5433/CMMI2022-9078012.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1586/9381233/f08bbd933664/CMMI2022-9078012.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1586/9381233/ee0daa2323b6/CMMI2022-9078012.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1586/9381233/2838af7294bc/CMMI2022-9078012.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1586/9381233/c371165d5433/CMMI2022-9078012.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1586/9381233/f08bbd933664/CMMI2022-9078012.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1586/9381233/ee0daa2323b6/CMMI2022-9078012.004.jpg

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本文引用的文献

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NTF4 stimulates the progression of gastric cancer via regulating FOXL1.NTF4 通过调控 FOXL1 促进胃癌的进展。
J BUON. 2021 Mar-Apr;26(2):499-505.
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