ArticleInternational journal of clinical and experimental pathology2019
miR-195 inhibits esophageal cancer cell proliferation and promotes apoptosis by downregulating YAP1.
Article in International journal of clinical and experimental pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Drug Delivery Opportunities in Esophageal Cancer: Current Treatments and Future Prospects.Molecular pharmaceutics · 2024Review
- ATG9A modulated by miR-195-5p can boost the malignant progression of cervical cancer cells.Epigenetics · 2023Article
- Smoking induces WEE1 expression to promote docetaxel resistance in esophageal adenocarcinoma.Molecular therapy oncolytics · 2023Article
- Sevoflurane Suppresses the Growth, Metastasis, and Invasion of Endometrial Carcinoma Cells via miR-195-5p/JAK2 Axis.Computational and mathematical methods in medicine · 2022Article
- RHO GTPase-Related Long Noncoding RNAs in Human Cancers.Cancers · 2021Review
- miRNAs Involved in Esophageal Carcinogenesis and miRNA-Related Therapeutic Perspectives in Esophageal Carcinoma.International journal of molecular sciences · 2021Review
- Approaches Toward Targeting Matrix Metalloproteases for Prognosis and Therapies in Gynecological Cancer: MicroRNAs as a Molecular Driver.Frontiers in oncology · 2021Review
- Expression and clinical significance of B cell translocation gene 2 in esophageal squamous cell carcinoma.International journal of clinical and experimental pathology · 2021Article
- Evaluation of the Diagnostic Potential of a Plasma Exosomal miRNAs Panel for Gastric Cancer.Frontiers in oncology · 2021Article
- Propofol Inhibits Proliferation and Invasion of Stomach Cancer Cells by Regulating miR-205/YAP1 Axis.Cancer management and research · 2020Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveYes-associated protein 1 (YAP1) regulates a variety of genes related to cell proliferation, cycle and apoptosis, and plays a role in the pathogenesis of esophageal cancer. It was found that the expression of miR-195 was significantly decreased in esophageal cancer tissues, suggesting its anti-cancer effect. Bioinformatics analysis revealed the targeted relationship between miR-195 and the 3'-UTR of YAP1. This study investigated the role of miR-195 in regulating YAP1 expression and affecting proliferation and apoptosis of esophageal cancer cells.
methodsThe tumor tissue and the adjacent tissue of patients with esophageal cancer were collected to detect the expressions of miR-195 and YAP1. Dual luciferase reporter gene assay was adopted to validate the targeted regulation between miR-195 and YAP1. Esophageal cancer EC9706 cells and normal esophageal epithelial HEEC cells were cultured in vitro to measure the expression of miR-195 and YAP1. EC9706 cells were divided into miR-NC group and miR-195 mimic group followed by analysis of cell apoptosis by flow cytometry and cell proliferation by EdU staining.
resultsCompared with adjacent tissues, miR-195 was significantly decreased, while YAP1 mRNA and protein were significantly upregulated in esophageal cancer tissues. Dual luciferase reporter gene assay confirmed that there was a targeted relationship between miR-195 and YAP1. Compared with HEEC cells, miR-195 expression was declined, whereas YAP1 was elevated in EC9706 cells. Transfection of miR-195 mimic significantly downregulated YAP1 expression, resulting in increased apoptosis and decreased proliferation of EC9706 cells.
conclusionDecreased expression of miR-195 plays a regulatory role in increasing YAP1 expression and promoting the pathogenesis of esophageal cancer. Elevation of miR-195 inhibites the expression of YAP1, restrains cell proliferation, and promotes cell apoptosis.
Indexed as
Identifiers
31933743PMC6943995W3017160514What 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.