ArticleBMC molecular and cell biology2022
MicroRNA-145-5p modulates Krüppel-like factor 5 and inhibits cell proliferation, migration, and invasion in nasopharyngeal carcinoma.
Article in BMC molecular and cell biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Harnessing miR-145 in NSCLC: mechanistic roles, diagnostic-prognostic utility, and therapeutic potential.Cancer cell international · 2025Review
- Dr. Jekyll or Mr. Hyde: The multifaceted roles of miR-145-5p in human health and disease.Non-coding RNA research · 2025Review
- lncRNA ENST00000422059 promotes cell proliferation and inhibits cell apoptosis in breast cancer by regulating the miR-145-5p/KLF5 axis.Acta biochimica et biophysica Sinica · 2023Article
- Targeting and delivery of microRNA-targeting antisense oligonucleotides in cardiovascular diseases.Atherosclerosis · 2023Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
backgroundIn several human cancers, Krüppel-like factor 5 (KLF5), a zinc finger transcription factor, can contribute to both tumor progression or suppression; however, the precise role of KLF5 in nasopharyngeal carcinoma (NPC) remains poorly understood. In this study, the association between KLF5 and microRNA-145-5p (miR-145-5p) in NPC cells was elucidated.
resultsOur results showed that KLF5 expression was up-regulated in NPC group compared to normal group. We found that KLF5 exhibited an oncogenic role in NPC cells. The upregulation of miR-145-5p inhibited the proliferation, migration, and invasion of NPC cells. It was observed that miR-145-5p could down-regulate the mRNA and protein expression of KLF5 in NPC cell lines. Additionally, the activity of focal adhesion kinase (FAK), a migration marker, was regulated by miR-145-5p and KLF5 in NPC cells.
conclusionsThe results of this study indicated that miR-145-5p could repress the proliferation, migration, and invasion of NPC cells via KLF5/FAK regulation, and could be a potential therapeutic target for patients with NPC.
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