Abstract
It has been previously reported that the long non-coding RNA nuclear enriched abundant transcript 1 (NEAT1) can regulate cell apoptosis. The present study aimed to investigate the involvement of NEAT1 in premature ovarian failure (POF). A total of 60 patients with POF admitted at the Sixth Affiliated Hospital of Sun Yat-sen University between December 2016 and December 2018 were enrolled in the present study. Reverse transcription-quantitative PCR (RT-qPCR) was performed to measure NEAT1 expression level in tissue samples from patients with POF and healthy controls. Transient transfections were performed on two normal Chinese hamster ovary cell lines Lec8 and CHO, followed by RT-qPCR and western blot to evaluate gene interaction. Flow cytometry was performed to assess cell apoptosis. The results from the present study demonstrated that NEAT1 expression in ovarian tissues was significantly downregulated in patients with POF compared with healthy controls. Furthermore, the expression of p53 was upregulated in ovarian tissues from patients with POF compared with healthy controls and was inversely associated with NEAT1 expression. In hamster ovary cells, overexpression of NEAT1 led to inhibition of p53, whereas NEAT1 knockdown promoted the expression of p53. In addition, ovary cell apoptosis was inhibited following NEAT1 overexpression and stimulated following p53 overexpression. In conclusion, overexpression of NEAT1 may inhibit the expression of p53 and improve premature ovarian failure.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.