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1.
Journal of Regional Anatomy and Operative Surgery ; (6): 241-244, 2015.
Article in Chinese | WPRIM | ID: wpr-500171

ABSTRACT

Objective To determine the roles and underlying molecular mechanism of MicroRNA-203 on the migration of human hypo-pharyngeal carcinoma cells. Methods The potential MicroRNA-203 target genes were searched by bioinformatic miRNA target prediction tools and KEGG database,and a large number of candidates was identified. The MEKK1 was selected for further investigation. This gene is known to play a role in tumor metastasis. The MicroRNA-203’s binding sites in MEKK1’s mRNA 3’UTR were analyzed by luciferase report-er assays. Nextly,the protein expression of MEKK1 in Fadu-Lv-MicroRNA-203 cells was determined by Western blot assay. The regulation of MEKK1’s mRNA expression by MicroRNA-203 was analyzed by qRT-PCR. Transwell cell migration assays were performed to confirm the im-pact of MicroRNA-203 on hypopharyngeal carcinoma metastasis. Results The expression level of endogenous MicroRNA-203 was negatively correlated with the mRNA and protein expression levels of MEKK1 in hypopharyngeal carcinoma cells. Transwell migration assay results showed that MicroRNA-203 overexpression inhibited hypopharyngeal carcinoma cell migration ability. Furtherly,MEKK1 can promote hypo-pharyngeal carcinoma cell migration ability. Conclusion MEKK1 is a direct target of MicroRNA-203. MicroRNA-203 plays a role in hypo-pharyngeal carcinoma cell migration ability through MEKK1.

2.
Journal of International Oncology ; (12): 419-421, 2013.
Article in Chinese | WPRIM | ID: wpr-433401

ABSTRACT

MicroRNA(miR)-203 is a stemness-inhibiting miRNA that adjusts the epithelioid cell differentiation by restricting the expression of stemness-related transcription factor.Its abnormal expression has been detected in several types of human cancers,including bladder cancer,breast cancer,colon cancer and pancreatic cancer.miR-203 plays a critical role in the tumor genesis and development by regulating cell proliferation,differentiation and apoptosis.

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