ArticleInternational journal of clinical and experimental pathology2018
MiR-361-5p decreases the tumorigenicity of epithelial ovarian cancer cells by targeting at RPL22L1 and c-Met signaling.
Article in International journal of clinical and experimental pathology, 2018. 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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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- Circular RNAs in EMT-driven metastasis regulation: modulation of cancer cell plasticity, tumorigenesis and therapy resistance.Cellular and molecular life sciences : CMLS · 2024Review
- Circ_0061140 Contributes to the Malignant Progression in Ovarian Cancer Cells by Mediating the RAB1A Level Through Sponging miR-361-5p.Biochemical genetics · 2022Article
- Alternative RNA splicing modulates ribosomal composition and determines the spatial phenotype of glioblastoma cells.Nature cell biology · 2022Article
- Construction of an Epithelial-Mesenchymal Transition-Related Model for Clear Cell Renal Cell Carcinoma Prognosis Prediction.Disease markers · 2022Article
- Exosomal long noncoding RNA HOXD-AS1 promotes prostate cancer metastasis via miR-361-5p/FOXM1 axis.Cell death & disease · 2021Article
- miR-361-5p regulates ovarian cancer cell proliferation and apoptosis by targeting TRAF3.Experimental and therapeutic medicine · 2021Article
- Article
- MicroRNA-361: A Multifaceted Player Regulating Tumor Aggressiveness and Tumor Microenvironment Formation.Cancers · 2019Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A large number of studies have shown that miRNAs are important regulators of epithelial-to-mesenchymal transition (EMT) and are associated with metastasis in epithelial ovarian cancer (EOC). MiR-361-5p has been shown to play pivotal roles in tumorigenesis and metastasis; however, a role for miR-361-5p in EOC has not been reported. In this study, we found that miR-361-5p was significantly down-regulated in EOC tissues and cell lines. In addition, over-expression of miR-361-5p inhibited the migration and invasion of EOC cells in vitro. MiR-361-5p influenced the expression of the EMT-associated proteins by upregulating the epithelial marker E-cadherin and downregulating the mesenchymal markers, N-cadherin and vimentin. Further studies identify miR-361-5p directly targeted Ribosomal L22-like1 (RPL22L1) and c-Met. Moreover, miR-361-5p repressed the Akt/mTOR pathway after c-Met inhibition. Reintroduction of RPL22L1 and c-Met reversed miR-361-5p-induced EMT suppression. Consistently, inverse correlations were also observed between the expression of miR-361-5p and RPL22L1 or c-Met in human EOC tissue samples. Taken together, miR-361-5p inhibited the EMT progression in EOC cells by targeting RPL22L1 and c-Met/Akt/mTOR signaling.
Indexed as
Identifiers
31938372PMC6958233W3027986955What OpenQuestion holds
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.