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Age-related cataract (ARC) is the primary cause of blindness worldwide. Abnormal expression of microRNAs (miRNAs/miRs) has been reported to be associated with multiple diseases, including ARC. However, the potential role of miR-124 in ARC remains unclear. The present study used the human lens epithelial cell line, SRA01/04, to investigate the potential role of miR-124 in ARC. Reverse transcription-quantitative PCR analysis was performed to detect the expression levels of miR-124, protein sprouty homolog 2 (SPRY2) and matrix metalloproteinase-2 (MMP-2) in ARC tissues, while western blotting was performed to detect the protein levels of SPRY2 and MMP-2. Cell viability and apoptosis of SRA01/04 cells were assessed via Cell Counting Kit-8 and TUNEL assays, respectively. The interaction between miR-124 and SPRY2 or MMP-2 was confirmed via the dual-luciferase reporter and RNA immunoprecipitation assays. The results of the present study demonstrated that miR-124 expression was significantly upregulated in ARC tissues, and knockdown of miR-124 increased SRA01/04 cell viability and suppressed apoptosis. In addition, SPRY2 and MMP-2 expression was decreased in ARC tissues, and were demonstrated to directly bind to miR-124. Overexpression of SPRY2 or MMP-2 increased SRA01/04 cell viability and repressed apoptosis, the effects of which were reversed following overexpression of miR-124. Taken together, these results suggested that miR-124 facilitates lens epithelial cell apoptosis by modulating SPRY2 or MMP-2 expression, providing a novel treatment approach for ARC. [ABSTRACT FROM AUTHOR]

The present study was designed to investigate the expression and function of transmembrane protein 16 (TMEM16A), a calcium-activated chloride channel (CaCC), in the stria vascularis (SV) of the cochlea of guinea pigs at different ages, and to understand the role of CaCCs in the pathogenesis of presbycusis (age-related hearing loss), the most common type of sensorineural hearing loss that occurs with natural aging. Guinea pigs were divided into the following groups: 2 weeks (young group), 3 months (youth group), 1 year (adult group), D-galactose intervention (D-gal group; aging model induced by subcutaneous injection of D-galactose) and T16Ainh-A01 (intraperitoneal injection of 50 µg/kg/day TMEM16A inhibitor T16Ainh-A01 for 2 weeks). Differences in the hearing of guinea pigs between the various age groups were analyzed using auditory brainstem response (ABR), and immunofluorescence staining was performed to detect TMEM16A expression in the SV and determine the distribution. Reverse transcription-quantitative PCR and western blot analyses were conducted to detect the mRNA and protein levels of TMEM16A in SV in the different age groups. Morris water maze behavior analysis demonstrated that spatial learning ability and memory were damaged in the D-gal group. Superoxide dismutase activity and malondialdehyde content assays indicated that there was oxidative stress damage in the D-gal group. The ABR thresholds gradually increased with age, and the increase in the T16Ainh-A01 group was pronounced. Immunofluorescence analysis in the cochlear SV of guinea pigs in different groups revealed that expression of TMEM16A increased with increasing age (2 weeks to 1 year); fluorescence intensity was reduced in the D-gal model of aging. As the guinea pigs continued to mature, the protein and mRNA contents of TMEM16A in the cochlea SV increased gradually, but were decreased in the D-gal group. The findings indicated that CaCCs in the cochlear SV of guinea pigs were associated with the development of hearing in guinea pigs, and that downregulation of TMEM16A may be associated with age-associated hearing loss. [ABSTRACT FROM AUTHOR]

Cervical cancer (CC) is one of the most frequent gynecological malignancies in females worldwide. Aberrant expression of microRNA (miR)-206 was reported to play an important role in tumor progression. The aim of the present study was to evaluate the potential role of miR-206 and verify its influence on the function of glucose-6-phosphate dehydrogenase (G6PD) in CC. Western blot analysis and RT-PCR were employed to measure miR-206 and G6PD expression. Luciferase assays were performed to validate G6PD as miR-206 targets. CCK-8 assay was performed to examine the regulation of miR-206 and G6PD on CC proliferation. The result showed that miR-206 was downregulated, while G6PD was upregulated in high risk human papillomavirus (HR-HPV)(+) CC. miR-206 directly targeted the 3′-UTR of G6PD. miR-206 overexpressed or G6PD low-expressed suppressed cell proliferation. miR-206 low expressed or G6PD overexpressed predicted poor prognosis. In conclusion, miR-206 reduced cancer growth and suppresses the G6PD expression in CC. This newly identified miR-206 may provide further insight into tumor progression and offers a promising target for the CC therapy. [ABSTRACT FROM AUTHOR]