ArticleInternational journal of clinical and experimental pathology2017
MiR-211 inhibits cell epithelial-mesenchymal transition by targeting MMP9 in gastric cancer.
Article in International journal of clinical and experimental pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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.
The trial behind it
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
4 citing papers in PubMed, 6 citations in OpenAlex.
- LncRNA MCM3AP-AS1 is downregulated in diabetic retinopathy and promotes cell apoptosis by regulating miR-211/SIRT1.Diabetology & metabolic syndrome · 2022Article
- Role and mechanism of miR-211 in human cancer.Journal of Cancer · 2022Review
- Review
- The Paradoxical Behavior of microRNA-211 in Melanomas and Other Human Cancers.Frontiers in oncology · 2020Review
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
Recent studies have demonstrated that the dysregulation of miRNAs are frequently associated with cancer progression including gastric cancer (GC). MiR-211 was found to act as tumor suppressor in GC, however, the functional role of miR-211 involved in GC cell epithelial-mesenchymal transition (EMT) process still to be investigated. In the study, we demonstrated that miR-211 was lower expression in gastric cancer tissues compared with adjacent normal tissues. Lower miR-211 expression was positively associated with distant metastasis and lymph node metastasis in GC patients. Survival curve by Kaplan-Meier method and log rank test revealed that lower miR-211 expression indicated a poor outcome in GC patients. Function assays showed that miR-211 inhibited cell invasion and cell epithelial-mesenchymal transition (EMT) process in GC by upregulating E-cadherin expression and down-regulating twist1 and N-cadherin expression. Furthermore, we demonstrated that miR-211 suppressed cell EMT by targeting MMP9 expression in GC. These results showed that miR-211 acted as a tumor suppressor in GC and may be a potential target of GC treatment.
Indexed as
Identifiers
31966599PMC6965239W3027415348What 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.