ArticleCancer medicine2018
FOXP3 inhibits MYC expression via regulating miR-198 and influences cell viability, proliferation and cell apoptosis in HepG2.
Article in Cancer medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 13 citations in OpenAlex.
- Regulatory T Cell Metabolism: A Promising Therapeutic Target for Cancer Treatment?Immune network · 2025Review
- miR-198 targetsFrontiers in oncology · 2024Article
- MicroRNAs as the Critical Regulators of Forkhead Box Protein Family in Pancreatic, Thyroid, and Liver Cancers.Biochemical genetics · 2023Review
- Long non-coding RNA ANRIL interacts with microRNA-34a and microRNA-125a, and they all correlate with disease risk and severity of Parkinson's disease.Journal of clinical laboratory analysis · 2022Article
- The promising role and prognostic value of miR-198 in human diseases.American journal of translational research · 2022Article
- Identification of genes, pathways and transcription factor-miRNA-target gene networks and experimental verification in venous thromboembolism.Scientific reports · 2021Article
- Sevoflurane represses the migration and invasion of gastric cancer cells by regulating forkhead box protein 3.The Journal of international medical research · 2021Article
- Nuclear FOXP3 inhibits tumor growth and induced apoptosis in hepatocellular carcinoma by targeting c-Myc.Oncogenesis · 2020Article
- Ubiquitin specific peptidase 19 is a prognostic biomarker and affect the proliferation and migration of clear cell renal cell carcinoma.Oncology reports · 2020Article
- ASCT2 overexpression is associated with poor survival of OSCC patients and ASCT2 knockdown inhibited growth of glutamine-addicted OSCC cells.Cancer medicine · 2020Article
- Self-Assembled Polysaccharide-Diphenylalanine/Au Nanospheres for Photothermal Therapy and Photoacoustic Imaging.ACS omega · 2019Article
- FOXP3 inhibits MYC expression via regulating miR-198 and influences cell viability, proliferation and cell apoptosis in HepG2.Cancer medicine · 2018Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveOur study aimed to explore the effects of FOXP3 expression on liver neoplasms cells and to further investigate the relationship between FOXP3 and proto-oncogene MYC.
methodsQRT-PCR was used for assessment of FOXP3 expression in liver neoplasms tissues and para-carcinoma tissues. The effects of FOXP3 on cell viability were determined by CCK8 assay, clone formation experiment, and flow cytometry. For miRNA selection, chips were used to figure out the differentially expressed miRNAs in FOXP3-overexpressing HepG2 cells. The result was followed by bioinformatics prediction to screen the possible MYC-targeted miRNAs, and it was examined by dual luciferase assay and ChIP assay. The expression levels of MYC protein and apoptosis-associated proteins (bcl2 and bax) were measured by Western blot assay.
resultsIt showed an under-regulated expression of FOXP3 in liver neoplasm tissues from qRT-PCR results. Overexpression of FOXP3 contributed to cell apoptosis as well as suppressed tumor cells' proliferation. MiR-198 was detected to be highly expressed in FOXP3-overexpressing HepG2 cells. FOXP3 regulated the transcription level of miR-198 by binding to its promoter sequence and overexpressed miR-198 could suppress tumor cells' proliferation and promote cell apoptosis. There existed targeted relationship between miR-198 and MYC gene. MiR-198 inhibited cancer by suppressing the expression of MYC in liver neoplasm.
conclusionFOXP3 up-regulated miR-198 expression by binding to its promoter sequence specifically, while miR-198 inhibited proto-oncogene MYC via targeted relationship. High level of miR-198 contributed to the apoptosis of tumor cells and suppressed cell viability meanwhile.
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