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miR-96-5p 通过抑制 FHL1 促进肺腺癌细胞表型。

MiR-96-5p Facilitates Lung Adenocarcinoma Cell Phenotypes by Inhibiting FHL1.

机构信息

Department of Respiratory Medicine, Changxing People's Hospital, Huzhou, Zhejiang Province, China 313100.

Department of Respiratory Medicine, The First People's Hospital of Huzhou, Huzhou, Zhejiang Province, China 313000.

出版信息

Comput Math Methods Med. 2022 Aug 16;2022:7891222. doi: 10.1155/2022/7891222. eCollection 2022.

DOI:10.1155/2022/7891222
PMID:36017148
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9398840/
Abstract

OBJECTIVE

FHL1 is understood as a tumor repressor gene in various cancers and a possible target for cancer treatment. We investigated the influences of FHL1 on cell functions as well as its molecular mechanisms in lung adenocarcinoma (LUAD) cells.

METHODS

The miRNA-mRNA modulatory axis was predicted by bioinformatics. The expression levels of FHL1 mRNA and protein in LUAD cells were, respectively, analyzed by qRT-PCR and western blot. Dual luciferase analysis was introduced to verify the interaction between miR-96-5p and FHL1. CCK-8, cell colony formation, and Transwell assays were utilized to analyze proliferation, colony formation, migration, and invasion of A549 cells.

RESULTS

Expression of FHL1 mRNA and protein in LUAD tissue and cells was downregulated, which was linked with poor prognoses of patients. In addition, FHL1 overexpression could hamper colony formation, proliferation, invasion, and migration of LUAD cells. In addition, dual-luciferase analysis verified miR-96-5p as an upstream regulator of FHL1. Overexpression of miR-96-5p suppressed FHL1 expression in LUAD cells and promoted proliferation, invasion, and migration of LUAD cells, while overexpression of FHL1 could simultaneously restore the above-mentioned promoting effect.

CONCLUSION

MiR-96-5p fostered cell malignant behaviors by targeting FHL1. This research uncovered the regulatory mechanism of FHL1 in LUAD and offered optional therapeutic targets for LUAD patients.

摘要

目的

FHL1 被认为是多种癌症中的肿瘤抑制基因，也是癌症治疗的潜在靶点。我们研究了 FHL1 对肺腺癌（LUAD）细胞功能的影响及其分子机制。

方法

通过生物信息学预测 miRNA-mRNA 调节轴。分别通过 qRT-PCR 和 Western blot 分析 LUAD 细胞中 FHL1 mRNA 和蛋白的表达水平。双荧光素酶分析用于验证 miR-96-5p 与 FHL1 之间的相互作用。CCK-8、细胞集落形成和 Transwell 分析用于分析 A549 细胞的增殖、集落形成、迁移和侵袭。

结果

LUAD 组织和细胞中 FHL1 mRNA 和蛋白的表达下调，与患者的预后不良相关。此外，FHL1 过表达可抑制 LUAD 细胞的集落形成、增殖、侵袭和迁移。此外，双荧光素酶分析验证了 miR-96-5p 是 FHL1 的上游调节因子。miR-96-5p 的过表达抑制了 LUAD 细胞中 FHL1 的表达，并促进了 LUAD 细胞的增殖、侵袭和迁移，而过表达 FHL1 可同时恢复上述促进作用。

结论

miR-96-5p 通过靶向 FHL1 促进细胞恶性行为。本研究揭示了 FHL1 在 LUAD 中的调控机制，为 LUAD 患者提供了可选的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9875/9398840/c7add5f1fafb/CMMM2022-7891222.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9875/9398840/ffd6ff64d073/CMMM2022-7891222.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9875/9398840/934c95fc735b/CMMM2022-7891222.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9875/9398840/a294f12e9b5d/CMMM2022-7891222.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9875/9398840/c7add5f1fafb/CMMM2022-7891222.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9875/9398840/ffd6ff64d073/CMMM2022-7891222.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9875/9398840/934c95fc735b/CMMM2022-7891222.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9875/9398840/a294f12e9b5d/CMMM2022-7891222.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9875/9398840/c7add5f1fafb/CMMM2022-7891222.004.jpg

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