ArticleOncology letters2019
miR-196a regulates the proliferation, invasion and migration of esophageal squamous carcinoma cells by targeting ANXA1.
Article in Oncology letters, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Article
- An overview of the regulatory role of annexin A1 in the tumor microenvironment and its prospective clinical application (Review).International journal of oncology · 2024Review
- Identification of oxidative stress-related biomarkers in uterine leiomyoma: a transcriptome-combined Mendelian randomization analysis.Frontiers in endocrinology · 2024Article
- Annexin A1 affects tumor metastasis through epithelial-mesenchymal transition: a narrative review.Translational cancer research · 2022Review
- MiR-196a promotes the proliferation and migration of esophageal cancer via the UHRF2/TET2 axis.Molecular and cellular biochemistry · 2022Article
- Liquid Biopsy in Squamous Cell Carcinoma of the Esophagus and of the Head and Neck.Frontiers in medicine · 2022Review
- Research on Correlations of miR-196a Expression with Progression and Prognosis of Cutaneous Squamous Cell Carcinoma.Clinical, cosmetic and investigational dermatology · 2022Article
- Review
- Review
- Overexpression of miR-518b in non-small cell lung cancer serves as a biomarker and facilitates tumor cell proliferation, migration and invasion.Oncology letters · 2020Article
- LncRNA SNHG1 regulates vascular endothelial cell proliferation and angiogenesis via miR-196a.Journal of molecular histology · 2020Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNA (miR)-196a is upregulated in various types of malignancy, including esophageal squamous cell carcinoma (ESCC); however, its role in ESCC is currently unclear. The present study aimed to investigate the biological role and molecular mechanism of miR-196a in ESCC. The expression levels of miR-196a in 25 tumor tissues and adjacent non-tumor tissues from patients with ESCC were measured by reverse transcription-quantitative polymerase chain reaction. In addition, miR-196a expression levels were assessed in the human normal esophageal epithelial cell line Het-1A and the ESCC cell line EC109. The effects of miR-196a on the proliferation, apoptosis, invasion and migration of EC109 cells were determined by MTT, flow cytometry and Transwell assays, respectively. A luciferase reporter assay and western blotting were performed to confirm the target gene of miR-196a, and to explore the molecular mechanism underlying the effects of miR-196a on regulation of ESCC cell phenotypes. The results demonstrated that miR-196a was markedly upregulated in ESCC tissues and EC109 cells. In addition, miR-196a downregulation suppressed EC109 cell proliferation, invasion and migration, but did not affect apoptosis. Annexin A1 (ANXA1) was demonstrated to be a direct target gene of miR-196a. ANXA1 protein knockdown reversed the effects of miR-196a inhibition on EC109 cell proliferation, invasion and migration. Furthermore, alongside the downregulation of miR-196a and the increase in ANXA1 expression, cyclooxygenase 2 (COX2), matrix metalloproteinase (MMP)-2 and Snail were downregulated, and E-cadherin was upregulated in EC109 cells. The results of the present study suggested that miR-196a may act as an oncogene in ESCC, and that miR-196a may regulate the proliferation, invasion and migration of ESCC cells by targeting ANXA1. Subsequently, ANXA1 may further modulate the expression levels of COX2, MMP-2, Snail and E-cadherin. In conclusion, the miR-196a/ANXA1 axis may represent a potential therapeutic target in ESCC.
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