Long non-coding RNA (lncRNA) AC026166.2-001 was found to be down-regulated in laryngeal squamous cell carcinoma (LSCC) tissues and metastatic neck lymph nodes. Decreased AC026166.2-001 was associated with poorer prognosis and may act as a novel biomarker for LSCC patients. In this study, AC026166.2–001 was overexpressed by a lentivirus vector and down-regulated by a small interfering RNA (siRNA). The results of real-time cell analysis (RTCA) and a plate colony formation assay showed that AC026166.2–001 inhibited LSCC cell proliferation and the clone-forming capacity. Cell cycle distribution and related protein changes were measured by flow cytometry. AC026166.2–001 arrested the cell cycle at the G1 phase and induced apoptosis. In addition, AC026166.2–001 decreased cell migration as measured by wound healing assays and transwell migration assays. Moreover, luciferase reporter assay and Western blotting results suggested that AC026166.2–001 acts as a sponge of miR-24-3p and regulates the expression of p27 and cyclin D1. The in vivo results showed that AC026166.2–001 significantly suppressed the growth of LSCC xenografts and promoted apoptosis. We validated the molecular mechanisms underlying AC026166.2–001 in LSCC. This is the first report of AC026166.2–001 acting as a tumor suppressor in LSCC by regulating the miR-24-3p/p27 axis.

BackgroundLZTS2 (leucine zipper tumor suppressor 2), a candidate tumor suppressor gene, suppresses cell growth and plays a vital role in the carcinogenesis and development of tumors. No studies to date have described methylation of the LZTS2 promoter in human cancers, including LSCC (laryngeal squamous cell carcinoma). Therefore, the aim of this study was to explore the relationship between LZTS2 promoter methylation and risk of LSCC.MethodsIn our study, LZTS2 promoter methylation levels in LSCC tumor and adjacent normal tissues from 96 patients were measured using quantitative methylation-specific polymerase chain reaction (qMSP) assays.ResultsThe qMSP analyses revealed that LZTS2 promoter methylation levels in the LSCC tumor samples were significantly higher than those in paired adjacent healthy tissue samples. Furthermore, LZTS2 methylation levels were elevated in smokers, advanced T classified, and clinically staged patients, as well as in patients with lymph node metastases. In addition, Kaplan-Meier survival curves results showed that overall survival of LSCC patients with hypomethylated LZTS2 promoters was significantly higher than that in patients with hyper-methylated LZTS2 promoters (log-rank test P = 0.028). Meanwhile, the area under the receiver operating characteristic curve was 0.920. The diagnostic threshold value for LZTS2 methylation was 11.63% (94.7% sensitivity and 80.4% specificity).ConclusionsLZTS2 promoter hypermethylation is associated with risk, progression, and prognosis of LSCC in a cohort of 96 human subjects; LZTS2 promoter hypermethylation is a candidate diagnostic and prognostic biomarker for LSCC.

Age-related hearing loss (ARHL) represents the frequently occurring disability that affects the elderly worldwide. The recent evidence has calculated ARHL to be most potential risk factor to predict dementia. β-amyloid plaques and tau accumulation in brain are hallmarks pathologic feature of Alzheimer’s disease (AD), which is a leading cause resulting in dementia. However, the potential mechanistic associations between ARHL and dementia remains unknown. We performed the present cross-sectional cohort study by enrolling 72 patients from research on hearing as well as the pathologic hallmarks of AD in brain. The exposure of hearing was measured by either word recognition score or mean pure-tone of the superior ear. The brain β-amyloid and tau standardized uptake value ratio (SUVR) were measured by positron emission tomography (PET). The covariates included gender, age, cardiovascular disease, education and hearing aid use. To analyze the association between hearing and β-amyloid/tau, linear regression was used and adjusted for potentially confounding covariates. Our data showed that the mean age was 67.1 ± 2.9 years. After adjusted for all the covariates, SUVR of β-amyloid showed an increase of 0.028 [95% confidence interval (CI) 0.004–0.061; P = 0.026], while that of tau exhibited an increase of 0.026 (95% CI 0.003–0.056; P = 0.033) per mean pure-tone increase by 10 dB (worsening). Likewise, per mean word-recognition score increase by 10%, the SUVR of β-amyloid showed an increase of 0.060 (95% CI 0.008–0.113; P = 0.023), while that of tau exhibited an increase of 0.059 (95% CI 0.009–0.111; P = 0.031). Taken together, our data demonstrates that hearing worsening was related to the increased burdens of β-amyloid as well as tau detected by PET, which were the AD pathological markers.

Background Estrogen‐related receptor gamma (ESRRG) has been identified as a tumor suppressor gene in several cancers. We aimed to evaluate ESRRG promoter methylation in laryngeal squamous cell carcinoma (LSCC) and its relative clinical value in LSCC. Methods Bisulfite pyrosequencing assays were performed on 91 pairs of tumor and paracancer tissues from LSCC patients in China. The diagnostic value and overall survival (OS) were analyzed descriptively by receiver operating characteristic (ROC) curves and the Kaplan‐Meier methods, respectively. Results The ESRRG promoter was more frequently hypermethylated in tumor tissues than in adjacent tissues (P < 0.01). ESRRG promoter methylation was significantly increased in advanced T stage tumors (P < 0.01) and advanced clinical stage patients (P < 0.01). Moreover, the area under the ROC curve (AUC) value (0.81) indicated high discrimination accuracy. Furthermore, ESRRG hypermethylation was associated with poor OS, as confirmed by Kaplan‐Meier survival curves (P < 0.01). Conclusion Our study indicated that ESRRG promoter hypermethylation contributed to LSCC‐related risks, primarily tumor progression and survival prognosis, in patients. ESRRG promoter methylation could, therefore, be a diagnostic and prognostic biomarker in LSCC.