ArticleExperimental and therapeutic medicine2017
MicroRNA-206 inhibits the viability and migration of medulloblastoma cells by targeting LIM and SH3 protein 1.
Article in Experimental and therapeutic medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- CircRNA and lncRNA-associated competing endogenous RNA networks in medulloblastoma: a scoping review.Cancer cell international · 2024Article
- Role of MicroRNAs in the Development and Progression of the Four Medulloblastoma Subgroups.Cancers · 2021Review
- Noncoding RNAs in pediatric brain tumors: Molecular functions and pathological implications.Molecular therapy. Nucleic acids · 2021Review
- miR-196B-5P and miR-200B-3P Are Differentially Expressed in Medulloblastomas of Adults and Children.Diagnostics (Basel, Switzerland) · 2020Article
- The Non-coding Side of Medulloblastoma.Frontiers in cell and developmental biology · 2020Review
- MicroRNA‑206 exerts anti‑oncogenic functions in esophageal squamous cell carcinoma by suppressing the c‑Met/AKT/mTOR pathway.Molecular medicine reports · 2019Article
- MicroRNA-206 suppresses proliferation and predicts poor prognosis of HR-HPV-positive cervical cancer cells by targeting G6PD.Oncology letters · 2018Article
- New Frontiers for the Cytoskeletal Protein LASP1.Frontiers in oncology · 2018Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNA (miR)-206 has been found to be deregulated in various types of human cancer, including medulloblastoma. However, the regulatory mechanism of miR-206 in medulloblastoma growth and metastasis remains largely unclear. In the present study, reverse transcription-quantitative polymerase chain reaction data indicated that miR-206 was significantly downregulated in medulloblastoma tissues compared with adjacent non-tumor tissues (P<0.01). Furthermore, low expression of miR-206 was significantly associated with seeding at presentation and anaplastic histology (P<0.01), but not with sex, age, or residual tumors. Overexpression of miR-206 significantly reduced the viability and migration of medulloblastoma D341 cells (P<0.01). LIM and SH3 protein 1 (LASP1) was further identified as a novel target of miR-206 in D341 cells. mRNA levels of LASP1 were significantly higher in medulloblastoma tissues compared to adjacent non-tumor tissues (P<0.01), with an inverse correlation to the miR-206 levels in medulloblastoma tissues. In addition, protein expression levels of LASP1 ere negatively regulated by miR-206 in D341 cells. Further investigation showed that overexpression of LASP1 significantly eliminated the inhibitory effects of miR-206 on the migration and invasion of D341 cells (P<0.01). In conclusion, our study demonstrates that miR-206 has a suppressive role in medulloblastoma cell viability and invasion, partly at least, via the targeting of LASP1. Our study highlights the importance of the miR-206/LASP1 in medulloblastoma.
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