ArticleMolecular cancer2016
MiR-143-3p functions as a tumor suppressor by regulating cell proliferation, invasion and epithelial-mesenchymal transition by targeting QKI-5 in esophageal squamous cell carcinoma.
Article in Molecular cancer, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 79 papers, 4 of them syntheses that pooled it.
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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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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
79 citing papers in PubMed, 4 syntheses or guidelines pooled it, 151 citations in OpenAlex.
- A systematic review, meta-analysis, and network analysis of diagnostic microRNAs in glaucoma.European journal of medical research · 2023Pooled it
- Prognostic value of micro-RNA 375, 133, 143, 145 in esophageal carcinoma: A systematic review and meta-analysis.Frontiers in oncology · 2022Pooled it
- Pooled it
- Prognostic Value of MicroRNAs in Esophageal Carcinoma: A Meta-Analysis.Clinical and translational gastroenterology · 2018Pooled it
- Hsa_circRNA_0101125 Promotes Proliferation, Migration, and Invasion of Esophageal Squamous Cell Carcinoma via miR-143-3p/ZNF148 Axis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- CXCL12-targeting siRNA nanoparticles alleviate immunosuppression and inhibit tumor progression in esophageal squamous cell carcinoma.Journal of nanobiotechnology · 2025Article
- Systematic exploration of prognostic alternative splicing events related to tumor immune microenvironment of Clear Cell Renal Cell Carcinoma.Cancer biomarkers : section A of Disease markers · 2025Article
- miR-124 inhibits the proliferation, migration and invasion of esophageal squamous cell carcinoma by downregulating STATS.American journal of translational research · 2025Article
- Hypoxia-induced miR-5100 promotes exosome-mediated activation of cancer-associated fibroblasts and metastasis of head and neck squamous cell carcinoma.Cell death & disease · 2024Article
- The multifaceted role of quaking protein in neuropsychiatric disorders and tumor progression.Frontiers in neuroscience · 2024Review
- miR-31/QKI-5 axis facilitates cell cycle progression of non-small-cell lung cancer cells by interacting and regulating p21 and CDK4/6 expressions.Cancer medicine · 2023Article
- CircBCAR3 accelerates esophageal cancer tumorigenesis and metastasis via sponging miR-27a-3p.Molecular cancer · 2022Article
- Comparative Profiling of Circulating Exosomal Small RNAs Derived From Peruvian Patients With Tuberculosis and Pulmonary Adenocarcinoma.Frontiers in cellular and infection microbiology · 2022Article
- LncRNA MEG3: Potential stock for precision treatment of cardiovascular diseases.Frontiers in pharmacology · 2022Review
- Review
- Circular RNA 0025984 Ameliorates Ischemic Stroke Injury and Protects Astrocytes Through miR-143-3p/TET1/ORP150 Pathway.Molecular neurobiology · 2021Article
- miRNA-Based Regulation of Alternative RNA Splicing in Metazoans.International journal of molecular sciences · 2021Review
- Quaking I-5 protein inhibits invasion and migration of kidney renal clear cell carcinoma via inhibiting epithelial-mesenchymal transition suppression through the regulation of microRNA 200c.Translational andrology and urology · 2021Article
- mi-IsoNet: systems-scale microRNA landscape reveals rampant isoform-mediated gain of target interaction diversity and signaling specificity.Briefings in bioinformatics · 2021Article
- Circular RNA circCSNK1G3 induces HOXA10 signaling and promotes the growth and metastasis of lung adenocarcinoma cells through hsa-miR-143-3p sponging.Cellular oncology (Dordrecht, Netherlands) · 2021Article
19 more citing papers are in PubMed but not listed here.
Corrections and comments
- Retraction · 2022-08-24Concerns/Issues about Data · Concerns/Issues about Image ·
- Retracted
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDysregulation of microRNAs (miRNAs) have been demonstrated to contribute to carcinogenesis. MiR-143-3p has been identified to function as a tumor suppressor in several tumors, but the role of miR-143-3p in esophageal squamous cell carcinoma (ESCC) has not been intensively investigated. Our aim was to evaluate the potential role of miR-143-3p in the progression of ESCC.
methodsThe expression levels of miR-143-3p and QKI-5 protein were measured in 80 resected ESCC tumor specimens and the clinicopathological significance of these levels determined. We also investigated the role of miR-143-3p in the regulation of QKI-5 expression in ESCC cell lines both in vivo and in vitro.
resultsMiR-143-3p levels were decreased in ESCC clinical samples and low expression of miR-143-3p was significantly associated with poor prognosis in ESCC patients. Ectopic expression of miR-143-3p suppressed proliferation and induced apoptosis in ESCC cells both in vivo and in vitro. Ectopic expression of miR-143-3p also reduced the metastatic potential of cells by selectively regulating epithelial-mesenchymal transition regulatory proteins. Furthermore, QKI-5 isoform was upregulated in ESCC tissues and was a direct target of miR-143-3p. Lastly, re-introduction of QKI-5 expression abrogated the inhibitory effects of miR-143-3p on ESCC cell proliferation and motility.
conclusionsOur results demonstrate that miR-143-3p acts as a tumor-suppressor by targeting QKI-5 in ESCC, suggesting that miR-143-3p is a potential therapy for the treatment of ESCC.
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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.