Development of a Serum-Free Culture Method for Endothelial Cells of the Stria Vascularis and Their Pro-Inflammatory Secretome Changes Induced by Oxidative Stress.

Objectives: Reactive oxygen species in the stria vascularis (SV) of the cochlea may be involved in the pathogenesis of sensorineural hearing loss. However, the effects of oxidative stress on SV endothelial cells (SV-ECs) remain largely unknown, and no feasible in vitro cell culture model exists for the functional study of SV-ECs.

Methods: We isolated primary SV-ECs from the SV of neonatal mice.

MicroRNA-182 regulates otocyst-derived cell differentiation and targets T-box1 gene.

Background: Recently, in vitro and in vivo models have identified that microRNAs (miRNAs), which are extensively expressed in the inner ear, play important roles in inner ear development and function. However, the function of miRNA in vertebrate tissue is not well understood.

Results: The current study used an in vitro model of embryonic mouse inner ear in a stem/progenitor cell culture to demonstrate that: 1) miR-182 is expressed during differentiation of inner ear stem/progenitor cell into a hair cell-like fate, 2) ectopic miR-182 promotes inner ear stem/progenitor cell differentiation into a hair cell-like fate, and 3) the function of miR-182 may be associated with its putative target Tbx1, a transcription factors that have been implicated in inner ear development and hair cell fate.

[DJ-1 expression in laryngeal squamous cell carcinoma and its relationship with tumor recurrence and metastasis].

Objective: To detect the expression of DJ-1 in laryngeal squamous cell carcinoma (LSCC) and to study the relationship between DJ-1 expression and clinical indexes of LSCC.

Methods: The expressions of DJ-1 protein in 71 LSCC samples and 9 cases control samples from laryngeal mucosa tissues of non-LSCC patients were detected using streptavidin peroxidase immunohistochemistry staining and the relationships between DJ-1 protein expression and clinicopathologic characteristics were analyzed.

Results: (1) The positive expression rate of DJ-1 protein in LSCC was 85.

MicroRNA expression in the embryonic mouse inner ear.

Although microRNA (miRNA) is expressed extensively in the postnatal mouse inner ear, its expression in the sensory epithelium during embryogenesis has not been well characterized. We investigated miRNA expression at E13.5 and E16.

Inhibition of Aurora-A suppresses epithelial-mesenchymal transition and invasion by downregulating MAPK in nasopharyngeal carcinoma cells.

Mitotic serine/threonine kinase Aurora-A (Aur-A) plays a critical role in regulating centrosome segregation and spindle assemble. Aur-A overexpression causes excessive centrosome duplication and abnormal spindle structure, leading to tumor malignant progression. Here, we investigated Aur-A expression in nasopharyngeal carcinoma (NPC) and the association between Aur-A and NPC invasiveness.

ZM 447439 inhibition of aurora kinase induces Hep2 cancer cell apoptosis in three-dimensional culture.

Mitotic Aurora kinases are essential for accurate chromosome segregation during cell division. Forced overexpression of Aurora kinase results in centrosome amplification and multipolar spindles, causing aneuploidy, a hallmark of cancer. ZM447439 (ZM), an Aurora selective ATP-competitive inhibitor, interferes with the spindle integrity checkpoint and chromosome segregation.

Aurora kinase inhibitory VX-680 increases Bax/Bcl-2 ratio and induces apoptosis in Aurora-A-high acute myeloid leukemia.

Previously, we and others showed that mitotic Aurora-A kinase (Aur-A) was required for accurate mitotic entry and proper spindle assembly. In this study, we found that expression of Aur-A was markedly elevated in bone marrow mononuclear cells (BMMCs) obtained from a significant portion of de novo acute myeloid leukemia (AML) patients. Targeting human primary AML cells with Aur-A kinase inhibitory VX-680 led to apoptotic cell death in a dose-dependent manner.

Aurora-A, a negative prognostic marker, increases migration and decreases radiosensitivity in cancer cells.

Centrosomal Aurora-A (Aur-A) kinase ensures proper spindle assembly and accurate chromosome segregation in mitosis. Overexpression of Aur-A leads to centrosome amplification, aberrant spindle, and consequent genetic instability. In the present study, Aur-A was found to be overexpressed in laryngeal squamous cell carcinoma (LSCC).