Dataset Information

MiR-369-3p participates in endometrioid adenocarcinoma via the regulation of autophagy.

ABSTRACT:

Background

The aim of this study is to examine miRNA profiling and miR-369-3p participates in endometrioid adenocarcinoma (EEC) via the regulation of autophagy.

Methods

EEC and its adjacent normal tissues were obtained from 20 clinical patients after surgery. MiRNA profiling was performed using next generation sequencing (NGS) and was validated with quantitative real time PCR (qRT-PCR). qRT-PCR was also employed to measure miR-369-3p and autophagy-related protein 10 (ATG10) expression levels. Western blotting assay was performed to measure the expressions of ATG10 and LC3B. Luciferase reporter assay was conducted to confirm the direct targeting of ATG10 by miR-369-3p. Cell proliferation and migration assays were utilized to analyze the role of miR-369-3p in HEC-1-A cells.

Results

We found that miR-369-3p expression levels were down-regulated in EEC compared to the control tissues. The overexpression of miR-369-3p inhibited cell proliferation and migration in EEC; furthermore, ATG10 expression increased in EEC tissues. ATG10 was found to be a potential target of miR-369-3p via a dual-luciferase reporter assay, and ATG10 was shown to be down-regulated by miR-369-3p in protein levels.

Conclusions

This study revealed that miR-369-3p inhibited cell proliferation and migration by targeting ATG10 via autophagy in EEC.

SUBMITTER: Liu P

PROVIDER: S-EPMC6624956 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Similar Datasets

Project description:Parkinson's disease (PD) can lead to movement injury and cognitive dysfunction. Although advances have been made in attenuating PD, the effect of inhibiting the development of PD remains disappointing. Therefore, the present study aimed at investigating the etiology of Parkinson's disease and developing an alternative therapeutic strategy for patients with PD. A PD mouse model was established using an intraperitoneal injection of 1‑methyl‑4‑phenyl‑1,2,3,6‑tetrahydropyridine hydrochloride (MPTP‑HCl; 30 mg/kg/day for 5 days), and a PD cellular model was established by treating SH‑SY5Y cells with different concentrations of 1‑methyl‑4‑phenylpyridinium (MPP+) for 24 h. The expression levels of circular RNA sterile α motif domain containing 4A (circSAMD4A) and microRNA (miR)‑29c‑3p in both midbrain tissues and SH‑SY5Y cells were detected via reverse transcription‑quantitative PCR. The interaction between circSAMD4A and miR‑29c‑3p was verified using a dual‑luciferase reporter experiment. Apoptosis‑, autophagy‑ and 5'AMP‑activated protein kinase (AMPK)/mTOR cascade‑associated proteins in midbrain tissues and SH‑SY5Y cells were detected using western blotting. Furthermore, TUNEL staining and flow cytometry were used to analyze cell apoptosis. It was found that circSAMD4A was upregulated, while miR‑29c‑3p was downregulated in both PD animal and cellular models. Moreover, circSAMD4A directly targeted and negatively regulated miR‑29c‑3p. Further studies identified that circSAMD4A knockdown inhibited MPTP‑ or MPP+‑induced apoptosis and autophagy; however, these effects were abolished by an miR‑29c‑3p inhibitor. In addition, circSAMD4A knockdown repressed phosphorylated‑AMPK expression and increased mTOR expression in MPTP‑ or MPP+‑induced PD models, the effects of which were reversed by a miR‑29c‑3p inhibitor. Collectively, these results suggested that circSAMD4A participated in the apoptosis and autophagy of dopaminergic neurons by modulating the AMPK/mTOR cascade via miR‑29c‑3p in PD.