ArticleExperimental and therapeutic medicine2021
Ultrasound-targeted microbubble destruction enhances the anti-tumor action of miR-4284 inhibitor in non-small cell lung cancer cells.
Article in Experimental and therapeutic medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Inhibition of miR-4284 could reduce apoptosis and neuroinflammation by targeting APBA1/JAK1/STAT3 signaling in Alzheimer's disease.Cell & bioscience · 2025Article
- STS-BN: An efficient Bayesian network method for detecting causal SNPs.Frontiers in genetics · 2022Article
- Construction and validation of a prognostic marker and risk model for HCC ultrasound therapy combined with WGCNA identification.Frontiers in genetics · 2022Article
- The Potential of Microbubbles as a Cancer Eradication Theranostic Agent.Pharmaceutical nanotechnology · 2022Review
- Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
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Abstract
MicroRNAs (miRNAs/miRs) are known to be involved in various human cancer types. Ultrasound-targeted microbubble destruction (UTMD) may improve the transfection efficiency of exogenous genes into target tissues and organs, thereby improving cancer treatment. In the present study, the role of miR-4284 in non-small cell lung cancer (NSCLC) was investigated and the effect of UTMD-mediated inhibition of miR-4284 on tumor progression was further analyzed. The expression of miR-4284 in NSCLC cells and tissues was detected by reverse transcription-quantitative PCR. UTMD-mediated inhibition of miR-4284 was achieved by co-transfection of microvesicles and miR-4284 inhibitors into NSCLC cells. A Cell Counting Kit-8 assay was used to determine NSCLC cell proliferation, and the migration and invasion of NSCLC cells were examined by Transwell assays. Compared with that in the control group, the expression of miR-4284 was increased in NSCLC tissues and cells. Knockdown of miR-4284 in NSCLC cells inhibited cell proliferation, migration and invasion. UTMD improved the transfection efficiency of miR-4284 inhibitors in NSCLC cells, resulting in more significant inhibition of tumor cell proliferation, migration and invasion. In conclusion, the results indicated that the expression of miR-4284 was increased in clinical samples and cell lines of NSCLC and that knockdown of miR-4284 inhibited the proliferation, migration and invasion of tumor cells. UTMD-mediated miR-4284 inhibition further promoted this effect, indicating that this technique may represent a novel strategy for the treatment of NSCLC.
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