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Updated: Aug 30, 2025
The Soft Agar Colony Formation Assay
Published on: October 27, 2014
MiR-96-5p Facilitates Lung Adenocarcinoma Cell Phenotypes by Inhibiting FHL1
Feng Zhou1, Chaojie Qian1, Tingting Chen1
1Department of Respiratory Medicine, Changxing People's Hospital, Huzhou, Zhejiang Province, China 313100.
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.
