c-Myc-Regulated lncRNA AFAP1-AS1 Promotes Proliferation of Oral Squamous Cell Carcinoma via the miR-655-3p/CCNA2 Axis.
TL;DR
Findings suggest that c-Myc-regulated AFAP1-AS1 may contribute to OSCC proliferation through modulation of the miR-655-3p/CCNA2 axis and provide insight into the molecular mechanisms underlying OSCC progression.
Abstract
Objective
This study aimed to investigate the molecular mechanisms by which AFAP1-AS1 promotes proliferation in oral squamous cell carcinoma (OSCC).
Materials And Methods
AFAP1-AS1 expression was examined in OSCC tissues and cell lines. Functional analyses were performed by silencing AFAP1-AS1 in vitro and assessing the resulting changes in CCNA2 expression. Bioinformatic analyses were used to predict microRNAs (miRNAs) potentially interacting with both AFAP1-AS1 and CCNA2, and these interactions were validated using dual-luciferase reporter assays and RNA immunoprecipitation (RIP). Chromatin immunoprecipitation (ChIP) assays were conducted to determine whether c-Myc directly binds to the AFAP1-AS1 promoter, thereby regulating its transcription.
Results
AFAP1-AS1 was significantly upregulated in OSCC tissues and cell lines compared with normal controls. Silencing AFAP1-AS1 led to decreased CCNA2 expression. Both computational predictions and experimental validations indicated that miR-655-3p interacts with AFAP1-AS1 and CCNA2, potentially acting as a regulatory intermediary. ChIP assays further showed that c-Myc directly binds to the promoter region of AFAP1-AS1, suggesting a role in its transcriptional activation.
Conclusion
These findings suggest that c-Myc-regulated AFAP1-AS1 may contribute to OSCC proliferation through modulation of the miR-655-3p/CCNA2 axis and provide insight into the molecular mechanisms underlying OSCC progression.