ArticleMolecular medicine reports2021
miR‑140‑5p inhibits the proliferation of multiple myeloma cells by targeting VEGFA.
Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 16 citations in OpenAlex.
- hsa_circ_0068631 facilitates the progression of diabetic retinopathy via regulating miR-140-5p in retinal microvascular endothelial cells.BMC ophthalmology · 2026Article
- Effects of mesenchymal stem cells from different sources on the biological functions of multiple myeloma cells.Stem cell research & therapy · 2025Article
- Dysregulation of Non-Coding RNAs: Roles of miRNAs and lncRNAs in the Pathogenesis of Multiple Myeloma.Non-coding RNA · 2023Review
- Role of microRNAs in B-Cell Compartment: Development, Proliferation and Hematological Diseases.Biomedicines · 2022Review
- MicroRNA-125a/b-5p promotes malignant behavior in multiple myeloma cells and xenograft tumor growth by targeting DIS3.The Kaohsiung journal of medical sciences · 2022Article
- Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNA (miR)‑140‑5p is associated with the growth and metastasis of various tumor cell types, yet its role in multiple myeloma (MM) remains unclear. Therefore, the present study aimed to investigate the regulatory effect of miR‑140‑5p on MM. Reverse transcription‑quantitative PCR analysis demonstrated that miR‑140‑5p was downregulated in MM cell lines, particularly in U266 and RPMI 8226 cells. A Cell Counting Kit‑8, wound healing and Transwell assays, as well as flow cytometry indicated that a miR‑140‑5p mimic could suppress cell viability, migration and invasion. In addition, the mimic promoted apoptosis of U266 and RPMI 8226 cells. Western blot data demonstrated that transfection with miR‑140‑5p mimic significantly reduced the expression levels of Ki‑67, cyclin D1, vimentin, Snail, matrix metalloproteinase (MMP)‑2 and MMP‑3. Moreover, as predicted by TargetScan7.2 and verified by luciferase activity assay, it was demonstrated that vascular endothelial growth factor A (VEGFA) was targeted by miR‑140‑5p. Further experiments indicated that VEGFA overexpression promoted cell viability, migration and invasion and suppressed apoptosis of MM cells, and that the miR‑140‑5p mimic partially reversed the effects of VEGFA overexpression. Therefore, miR‑140‑5p suppressed MM progression by targeting VEGFA. The present findings provide insight into potential therapeutic strategies for the treatment of MM.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.