ArticleInternational journal of clinical and experimental pathology2017
miR-222 knockdown suppresses epithelial-to-mesenchymal transitionin human oral squamous cell carcinoma.
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 3 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
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- Nutlin-3 suppresses tumorigenesis and progression of oral squamous cell carcinoma and enhances chemosensitivity to cisplatin.Cytotechnology · 2023Article
- FERMT1 knockdown inhibits oral squamous cell carcinoma cell epithelial-mesenchymal transition by inactivating the PI3K/AKT signaling pathway.BMC oral health · 2021Article
- Extracellular Vesicle-Mediated Chemoresistance in Oral Squamous Cell Carcinoma.Frontiers in molecular biosciences · 2021Review
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
Tumor metastasis is the main cause of death in patients with oral squamous cell carcinoma (OSCC). Epithelial-to-mesenchymal transition (EMT) is potentially associated with metastasis and histological grading in OSCC. Therefore, the discovery of new strategies to inhibit EMT is potentially valuable for the development of therapies for OSCC. In our previous study, we found that miR-222, which is up-regulated in OSCC, regulates the biological behavior of OSCC cells by targeting the p53-upregulated modulator of apoptosis (PUMA); however, the effect of miR-222 on TGF-β1-induced EMT in OSCC cells is unclear. In this study, OSCC cell lines CAL-27 and Tca-8113 were incubated with 5 ng/ml of TGF-β1 to inhibit the expression of E-cadherin, promote the expression of N-cadherin, vimentin, and α-SMA and stimulate achange in cell shape convert from a "cuboidal" epithelial structure into an elongated mesenchymal shape. We found that the expression of miR-222 was up-regulated during TGF-β1-induced EMT in OSCC cells. In addition, miR-222 knockdown reversed TGF-β1-induced EMT by targeting PUMA. Our findings indicate that miR-222 plays an important role in OSCC, potentially serving as a novel therapeutic target for the treatment of OSCC.
Indexed as
Identifiers
31966478PMC6965878W3026531284What 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.