학술논문
AC092127.1-miR-451a-AE binding protein 2 Signaling Facilitates Malignant Properties of Breast Cancer
Document Type
Article
Author
Source
(2021): 389-401.
Subject
Language
Korean
ISSN
17386756
Abstract
Purpose: The purpose of the current study was to explore the functions and potential mechanism of miR-451a in breast cancer (BC). Methods: Quantitative reverse transcription real-time polymerase chain reaction was used to analyze the expression of miR-451a in human normal mammary cells (MCF-10A) and BC cells. Colony formation assay, terminal-deoxynucleoitidyl transferase mediated nick end labeling assay and transwell assays were conducted to validate the effect of miR-451a on proliferation, apoptosis, migration and invasion of BC cells, respectively. RNA pull-down, RNA immunoprecipitation and luciferase reporter assays were applied to investigate the upstream and downstream mechanisms of miR-451a in BC cells. Results: MiR-451a was expressed at a low level in BC cells. Overexpression of miR-451a repressed BC cells proliferation, migration and invasion. Moreover, long non-coding RNA AC092127.1 acted as a sponge of miR-451a to enhance the expression level of AE binding protein 2 (AEBP2) that was demonstrated to be the target gene of miR-451a in BC cells. Finally, rescue experiments validated that miR-451a and AEBP2 involved in AC092127.1-mediated BC cell growth, migration and invasion. Conclusion: In a word, AC092127.1/miR-451a/AEBP2 axis contributes to BC cell growth, migration and invasion. Our results may help to find novel potential targets for BC treatment.
Purpose: The purpose of the current study was to explore the functions and potential mechanism of miR-451a in breast cancer (BC). Methods: Quantitative reverse transcription real-time polymerase chain reaction was used to analyze the expression of miR-451a in human normal mammary cells (MCF-10A) and BC cells. Colony formation assay, terminal-deoxynucleoitidyl transferase mediated nick end labeling assay and transwell assays were conducted to validate the effect of miR-451a on proliferation, apoptosis, migration and invasion of BC cells, respectively. RNA pull-down, RNA immunoprecipitation and luciferase reporter assays were applied to investigate the upstream and downstream mechanisms of miR-451a in BC cells. Results: MiR-451a was expressed at a low level in BC cells. Overexpression of miR-451a repressed BC cells proliferation, migration and invasion. Moreover, long non-coding RNA AC092127.1 acted as a sponge of miR-451a to enhance the expression level of AE binding protein 2 (AEBP2) that was demonstrated to be the target gene of miR-451a in BC cells. Finally, rescue experiments validated that miR-451a and AEBP2 involved in AC092127.1-mediated BC cell growth, migration and invasion. Conclusion: In a word, AC092127.1/miR-451a/AEBP2 axis contributes to BC cell growth, migration and invasion. Our results may help to find novel potential targets for BC treatment.
Purpose: The purpose of the current study was to explore the functions and potential mechanism of miR-451a in breast cancer (BC). Methods: Quantitative reverse transcription real-time polymerase chain reaction was used to analyze the expression of miR-451a in human normal mammary cells (MCF-10A) and BC cells. Colony formation assay, terminal-deoxynucleoitidyl transferase mediated nick end labeling assay and transwell assays were conducted to validate the effect of miR-451a on proliferation, apoptosis, migration and invasion of BC cells, respectively. RNA pull-down, RNA immunoprecipitation and luciferase reporter assays were applied to investigate the upstream and downstream mechanisms of miR-451a in BC cells. Results: MiR-451a was expressed at a low level in BC cells. Overexpression of miR-451a repressed BC cells proliferation, migration and invasion. Moreover, long non-coding RNA AC092127.1 acted as a sponge of miR-451a to enhance the expression level of AE binding protein 2 (AEBP2) that was demonstrated to be the target gene of miR-451a in BC cells. Finally, rescue experiments validated that miR-451a and AEBP2 involved in AC092127.1-mediated BC cell growth, migration and invasion. Conclusion: In a word, AC092127.1/miR-451a/AEBP2 axis contributes to BC cell growth, migration and invasion. Our results may help to find novel potential targets for BC treatment.