Abstract
Purpose
Although SLC16A1-AS1 is involved in lung cancer, its function in breast cancer is still elusive. We observed downregulation of SLC16A1-AS1 expression in triple-negative breast cancer (TNBC) by analyzing TCGA dataset. Therefore, we analyzed the function of SLC16A1-AS1 in TNBC.
Methods
We observed downregulation of SLC16A1-AS1 expression in TNBC by analyzing TCGA dataset. Therefore, we analyzed the function of SLC16A1-AS1 in TNBC.
Results
SLC16A1-AS1 expression was downregulated in TNBC tissues. SLC16A1-AS1 interacted with miR-182, whereas SLC16A1-AS1 and miR-182 overexpression failed to affect their expression. SLC16A1-AS1 overexpression upregulated the expression of PDCD4, a downstream target of miR-182. SLC16A1-AS1 and PDCD4 overexpression suppressed cell cycle progression from the G1 phase to the G2 phase. MiR-182 and silencing of PDCD4 played the opposite role. Additionally, miR-182 overexpression inhibited the role of SLC16A1-AS1 overexpression on cell cycle progression in both BT-549 and BT20 cells. The cell proliferation assay showed that SLC16A1-AS1 and PDCD4 overexpression decreased the cell proliferation rate.
Conclusion
SLC16A1-AS1 may inhibit cell cycle progression and restrain TNBC cell proliferation by regulating the miR-182/PDCD4 axis.
Authors’ contributions
Li: study concepts, study design, literature research, experimental studies, manuscript preparation and editing; Jiang and Liu: definition of intellectual content, literature research experimental studies, manuscript preparation and editing; Gai and Guan: literature research and experiments work; All authors read and approved the final manuscript.
Ethics approval and consent to participate
Ethical approval was obtained from the Ethics Committee of College of Basic Medical Sciences, China Medical University. Written informed consent was obtained from all individual patients included in the study.
Disclosure statement
The authors declare that they have no competing interests.
Data availability statement
The datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request.