Comprehensive analysis of the immune implication of EPHX4 gene in laryngeal squamous cell carcinoma.

OBJECTIVES: The role of Epoxide Hydrolase-4 (EPHX4), a member of epoxide hydrolase family, has not been investigated in cancer. The purpose of this article is to explore the application value of EPHX4 in laryngeal cancer and its relationship with immune infiltration. METHODS: We observed that EPHX4 expression and its survival assays in laryngeal cancer specimens based on The Cancer Genome Atlas (TCGA) cohorts. We also analyzed the correlation between immune cell infiltration levels and EPHX4 gene copy number in laryngeal cancer. Finally, we conducted in vitro assay to evaluate the functions of EPHX4 in laryngeal cancer cell line. RESULTS: EPHX4 is highly expressed in laryngeal cancer specimens and has a poor prognosis. EPHX4 related immune cell analysis showed that it participated in NK Natural killer cell mediated cytotoxicity. Finally, Cell experiments indicate that EPHX4 could promote laryngeal cancer cell line proliferation, colony formation and invasion. CONCLUSIONS: Our research results suggest that EPHX4 may be a potential immunotherapy target for laryngeal cancer. The nominated immune signature is a helpful and promising prognostic indicator in laryngeal cancer. LEVELS OF EVIDENCE: Level 3.

The correlation of plasma omentin-1 with insulin resistance in non-obese polycystic ovary syndrome.

OBJECTIVES: Aberrant circulating adipokines are considered to be related to the pathological mechanism of polycystic ovary syndrome (PCOS). This study aims to evaluate the relationship between plasma omentin-1 levels, metabolic and hormonal parameters in the setting of non-obese Chinese women with PCOS. MATERIAL AND METHODS: This was a case-controlled, cross-sectional study of 153 non-obese (BMI<25kg/m(2)) PCOS and 114 age-matched healthy non-obese control individuals. Levels of plasma omentin-1, fasting blood glucose, insulin and sexual hormones and ovary volume were analyzed in all subjects. RESULTS: Plasma omentin-1 levels of non-obese PCOS individuals were significantly lower than in healthy non-obese controls. Body Mass Index (BMI), homeostasis model of assessment for insulin resistance index (HOMA-IR), levels of testosterone, luteinizing hormone (LH) and follicle-stimulating hormone (FSH), LH/FSH ratio and ovary volume (OV) were significantly higher in subjects with PCOS than controls. In the HOMA-IR stratified subgroups, PCOS individuals with insulin resistance had lower omentin-1 than those without insulin resistance after BMI adjustment. Omentin-1 was negatively correlated with BMI, HOMA-IR and fasting insulin. Multiple linear regressions revealed that BMI contributed to omentin-1 levels. Ovary volume was negatively correlated to HOMA-IR but had no correlation with omentin-1. CONCLUSIONS: Plasma omentin-1 concentrations were decreased in the non-obese PCOS group. Insulin resistance could further decrease plasma omentin-1 in non-obese individuals with PCOS independent of BMI status.

[Mutational analysis of candidate genes in a Chinese pedigree with dominantly inherited auditory neuropathy].

OBJECTIVE: Three genes including the OTOF, the DFNB59 and the DIAPH3 have been implicated previously in human non-syndromic auditory neuropathy. In this study, we aim to investigate whether DIAPH3 gene or the known deafness loci of 25 cloned autosomal dominant deafness (DFNA) genes contribute to the nonsyndromic hearing loss of a Chinese pedigree with dominantly inherited auditory neuropathy (AN). METHOD: Nine members of the kernal pedigree in this family were selected. Genomic DNA was isolated from the peripheral leukocytes of the subjects using the Puregene DNA Isolation Kits. Firstly, the 5'UTR of DIAPH3 gene was PCR amplified in all subjects. Then, the DNA fragments spanning the entire coding regions of DIAPH3, GJB2 and GJB3 genes, and 50 exons in other 23 cloned DFNA genes were amplified using specific primers. Each fragment was purified and analyzed by direct sequencing. The resultant sequence data were compared with the standard sequence to identify deafness-associated mutations. RESULT: PCR amplifications were successfully conducted. We failed to detect the presence either of c. --172G > A mutation in the 5'UTR that have been reported, or any other deafness-associated mutations in the whole DIAPH3 gene, by sequence analysis. We also did not find any known deafness-causing mutations among the 25 cloned DFNA genes. CONCLUSION: The DIAPH3 gene, and the known deafness loci of 25 cloned DFNA genes seem not contribute to the pathogenesis of this Chinese AN family in this study, which suggesting new gene(s) involvement.