BackgroundIt was previously reported that downregulation of miR-218 promoted thyroid cancer cell invasion, migration, and proliferation. However, the biological functions of miR-218 and its possible regulatory mechanisms in papillary thyroid cancer (PTC) cells are still elusive.Materials and methodsThe expression levels of miR-218 and Runx2 in PTC tissues and cells were determined by quantitative real-time PCR (qRT-PCR) and Western blot. The effects of miR-218 overexpression on cell viability, invasion, apoptosis, and PTEN/PI3K/AKT pathway in PTC cells were evaluated by cell counting kit-8 assay, Transwell invasion assay, flow cytometry assay, and Western blot, respectively. Luciferase reporter assay and qRT-PCR were performed to identify the target of miR-218. Xenograft tumor experiment was performed to confirm the biological roles of miR-218 and its potential mechanisms in vivo.ResultsmiR-218 expression was downregulated and Runx2 expression was upregulated in PTC tissues and cells. Overexpression of miR-218 suppressed viability and invasion, and induced apoptosis of PTC cells in vitro, while Runx2 overexpression greatly abolished these effects. miR-218 overexpression inactivated the PTEN/PI3K/AKT pathway, which was abated by Runx2 upregulation. Additionally, Runx2 was validated to be a direct target of miR-218. Moreover, enforced expression of miR-218 inhibited tumor growth and Runx2 expression, and blocked PTEN/PI3K/AKT pathway in vivo.ConclusionmiR-218 overexpression suppresses the tumorigenesis of PTC via downregulating PTEN/PI3K/AKT pathway by targeting Runx2, which indicates that miR-218 may be a potential therapeutic target for human PTC.

This study revealed for the first time the protective effects of hydrogen-saturated saline on noise-induced hearing loss (NIHL) are related to both the anti-oxidative activity and anti-inflammatory activity.

This is the first study to clarify the correlations between different GJB2 biallelic genotypes and NSSHI phenotype in the Chinese population. The Chinese subjects with two truncating mutations in GJB2 were shown to correlate with more severe HI.

Background:The molecular genetic research showed the association between X-linked hearing loss and mutations in POU3F4. This research aimed to identify a POU3F4 mutation in a nonsyndromic X-linked recessive hearing loss family.Methods:A series of clinical evaluations including medical history, otologic examinations, family history, audiologic testing, and a high-resolution computed tomography scan were performed for each patient. Bidirectional sequencing was carried out for all polymerase chain reaction products of the samples. Moreover, 834 controls with normal hearing were also tested.Results:The pedigree showed X-linkage recessive inheritance pattern, and pathogenic mutation (c.499C>T) was identified in the proband and his family member, which led to a premature termination prior to the entire POU domains. This mutation co-segregated with hearing loss in this family. No mutation of POU3F4 gene was found in 834 controls.Conclusions:A nonsense mutation is identified in a family displaying the pedigree consistent with X-linked recessive pattern in POU3F4 gene. In addition, we may provide molecular diagnosis and genetic counseling for this family.