ArticleMolecular medicine reports2017
miR‑34c‑3p acts as a tumor suppressor gene in osteosarcoma by targeting MARCKS.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Immunotherapy in pediatric bone sarcomas: Current progress and future directions.Human vaccines & immunotherapeutics · 2026Review
- Antitumor effects of chemically modified miR-143 lipoplexes in a mouse model of pelvic colorectal cancer via myristoylated alanine-rich C kinase substrate downregulation.Molecular therapy. Nucleic acids · 2023Article
- Jaceosidin inhibits the progression and metastasis of NSCLC by regulating miR-34c-3p/Integrin α2β1 axis.Heliyon · 2023Article
- Small Extracellular Vesicles Containing miR-34c Derived from Bone Marrow Mesenchymal Stem Cells Regulates Epithelial Sodium Channel via Targeting MARCKS.International journal of molecular sciences · 2022Article
- Article
- METTL14-Mediated miR-30c-1-3p Maturation Represses the Progression of Lung Cancer via Regulation of MARCKSL1 Expression.Molecular biotechnology · 2022Article
- The myristoylated alanine-rich C-kinase substrates (MARCKS): A membrane-anchored mediator of the cell function.Autoimmunity reviews · 2021Review
- Long non‑coding RNA H19 regulates LASP1 expression in osteosarcoma by competitively binding to miR‑29a‑3p.Oncology reports · 2021Article
- MARCKSL1 promotes the proliferation, migration and invasion of lung adenocarcinoma cells.Oncology letters · 2020Article
- miRNA signatures in childhood sarcomas and their clinical implications.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2019Review
- MARCKS and Lung Disease.American journal of respiratory cell and molecular biology · 2019Review
- Knockdown of the oncogene lncRNA NEAT1 restores the availability ofBioscience reports · 2018Article
Corrections and comments
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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
Previous studies have demonstrated that microRNA (miR)‑34c‑3p is important in human cancer progression. However, the function of miR‑34c‑3p in osteosarcoma (OS) remains to be elucidated. In the present study, miR‑34c‑3p level was measured by reverse transcription‑quantitative polymerase chain reaction in OS tissues and the associated prognostic value for overall survival was determined. The function of miR‑34c‑3p was examined in vitro and in vivo. A luciferase reporter assay was used to identify the targets of miR‑34c‑3p. The results of the present study revealed that miR‑34c‑3p was downregulated in OS tissues and cell lines, and decreased levels of miR‑34c‑3p were associated with a high mortality rate in patients with OS. Furthermore, restoration of miR‑34c‑3p expression reduced cell growth in vitro and suppressed tumorigenesis in vivo. Conversely, inhibition of miR‑34c‑3p stimulated OS cell growth in vitro and in vivo. Myristoylated alanine‑rich protein kinase C substrate (MARCKS) was identified as a direct target of miR‑34c‑3p and its overexpression partly reversed the suppressive effects of miR‑34c‑3p. Furthermore, MARCKS was revealed to be upregulated and inversely correlated with miR‑34c‑3p levels in OS tissues. These data suggested that miR‑34c‑3p acts as a tumor suppressor via regulation of MARCKS expression in OS progression and miR‑34c‑3p may be a promising therapeutic target for this type of cancer.
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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.