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Silencing of lncRNA TFAP2A‑AS1 attenuates the development of acute coronary syndrome by inhibiting TFAP2A expression

  • Authors:
    • Shiwei Huang
    • Fanlu Guan
    • Fanhao Ye
    • Bozhi Ye
    • Sisi Han
    • Hao Chen
  • View Affiliations / Copyright

    Affiliations: Department of Cardiovascular Medicine, Wenzhou People's Hospital, Wenzhou, Zhejiang 325000, P.R. China, Department of Cardiovascular Medicine, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, P.R. China
    Copyright: © Huang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 20
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    Published online on: November 26, 2025
       https://doi.org/10.3892/br.2025.2093
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Abstract

Acute coronary syndrome (ACS), the acute manifestation of ischemic heart disease, remains a major cause of morbidity and mortality worldwide. The present study aimed to elucidate the preliminarily biological role and underlying mechanism of the long non‑coding RNA (lncRNA) transcription factor AP‑2α (TFAP2A)‑AS1 in ACS. The viability, apoptosis, invasion, and migration of human coronary artery endothelial cells (HCAECs) were assessed using Cell Counting Kit‑8, flow cytometric, Transwell, and wound healing assays. In addition, reverse transcription‑quantitative PCR was performed to examine the expression levels of TFAP2A‑AS1 and TFAP2A. Western blotting was performed to determine the protein level of TFAP2A. Furthermore, a mouse model of ACS was established to investigate the effects of TFAP2A‑AS1 and TFAP2A on blood lipid levels. Histological changes were evaluated through hematoxylin and eosin staining. The results revealed high levels of TFAP2A‑AS1 and TFAP2A expression in patients with ACS and in mouse models. In HCAECs, knockdown of TFAP2A‑AS1 resulted in decreased TFAP2A expression, whereas silencing of TFAP2A did not affect the expression of TFAP2A‑AS1. Interference with either TFAP2A‑AS1 or TFAP2A in HCAECs led to suppressed cell viability, invasion, and migration, as well as an increased apoptosis rate. Furthermore, it was demonstrated that the absence of both TFAP2A‑AS1 and TFAP2A reduced blood lipid levels and improved myocardial injury in a mouse model of ACS. In conclusion, groundbreaking findings revealed that the suppression of TFAP2A‑AS1 could effectively mitigate the progression of ACS by reducing the expression of TFAP2A. This finding not only offers crucial insight into the pathogenesis of ACS but also provides a solid theoretical foundation for the development of novel therapeutic interventions in clinical settings.
View Figures

Figure 1

Serum from patients with ACS exhibits
elevated expression levels of TFAP2A-AS1 and TFAP2A. The expression
of (A) TFAP2A-AS1 and (B) TFAP2A in patients with ACS and healthy
individuals was detected by reverse transcription-quantitative PCR.
***P<0.001 vs. Healthy. ACS, acute coronary syndrome;
TFAP2A, transcription factor AP-2α.

Figure 2

Silencing of TFAP2A-AS1 suppresses
TFAP2A expression. (A) The expression of TFAP2A-AS1 in HCAECs after
transfection with TFAP2A-AS1 siRNA1/2/3 or NC siRNA was detected by
RT-qPCR. ***P<0.001 vs. NC siRNA. (B) The expression
of TFAP2A in HCAECs after transfection with TFAP2A siRNA1/2/3 or NC
siRNA was detected by RT-qPCR. ***P<0.001 vs. NC
siRNA. (C) The expression of TFAP2A-AS1 and TFAP2A in HCAECs after
transfection with TFAP2A-AS1 siRNA, TFAP2A siRNA or NC siRNA was
detected by RT-qPCR. ***P<0.001 vs. NC siRNA. (D) The
protein levels of TFAP2A in HCAECs after transfection with
TFAP2A-AS1 siRNA, TFAP2A siRNA or NC siRNA were determined using
western blotting. **P<0.01 and
***P<0.001 vs. NC siRNA. (E) RIP assay demonstrated
an enrichment of TFAP2A-AS1. ***P<0.001 vs. anti-IgG.
(F) RNA pull-down assay showed that TFAP2A interacting with
biotin-labeled TFAP2A-AS1 was higher than that with the antisense
of TFAP2A-AS1 group. TFAP2A, transcription factor AP-2α; HCAECs,
human coronary artery endothelial cells; siRNA, small interfering
RNA; NC, negative control; RT-qPCR, reverse
transcription-quantitative PCR; RIP, RNA immunoprecipitation; ns,
no significance.

Figure 3

Silencing of TFAP2A-AS1 and TFAP2A
suppresses the proliferative, migratory, and invasive capacities
while enhancing the apoptotic rate of HCAECs. (A) The apoptosis
rate, (B) viability, (C) invasion and (D) migration of HCAECs
transfected TFAP2A-AS1 siRNA, TFAP2A siRNA or NC siRNA was assessed
by flow cytometric analysis, Counting Kit-8 assay, Transwell
invasion assay and wound healing assay, respectively. Scale bar,
100 µm. ***P<0.001 vs. NC siRNA. TFAP2A,
transcription factor AP-2α; HCAECs, human coronary artery
endothelial cells; siRNA, small interfering RNA; NC, negative
control.

Figure 4

Knockdown of TFAP2A-AS1 and TFAP2A
leads to a reduction in serum lipid levels and an improvement in
myocardial injury in an ACS mouse model. (A) The expression of
TFAP2A-AS1 and TFAP2A in ACS mice after injection of TFAP2A-AS1
shRNA, TFAP2A shRNA or NC shRNA was detected by reverse
transcription-quantitative PCR. (B) The protein levels of TFAP2A in
ACS mice after injection of TFAP2A-AS1 shRNA, TFAP2A shRNA or NC
shRNA were determined using western blotting. (C) The levels of TC,
LDL-C and HDL-C in ACS mice after injection of TFAP2A-AS1 shRNA,
TFAP2A shRNA or NC shRNA were determined using biochemical tests.
(D) Hematoxylin and eosin staining was performed to observe the
pathological condition of myocardial tissues in different groups.
Scale bar, 50 µm. ***P<0.001 vs. sham;
#P<0.05, ##P<0.01, and
###P<0.001 vs. the ACS model + NC shRNA. TFAP2A,
transcription factor AP-2α; ACS, acute coronary syndrome; shRNA,
short hairpin RNA; ns, no significance.
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Spandidos Publications style
Huang S, Guan F, Ye F, Ye B, Han S and Chen H: Silencing of lncRNA TFAP2A‑AS1 attenuates the development of acute coronary syndrome by inhibiting TFAP2A expression. Biomed Rep 24: 20, 2026.
APA
Huang, S., Guan, F., Ye, F., Ye, B., Han, S., & Chen, H. (2026). Silencing of lncRNA TFAP2A‑AS1 attenuates the development of acute coronary syndrome by inhibiting TFAP2A expression. Biomedical Reports, 24, 20. https://doi.org/10.3892/br.2025.2093
MLA
Huang, S., Guan, F., Ye, F., Ye, B., Han, S., Chen, H."Silencing of lncRNA TFAP2A‑AS1 attenuates the development of acute coronary syndrome by inhibiting TFAP2A expression". Biomedical Reports 24.2 (2026): 20.
Chicago
Huang, S., Guan, F., Ye, F., Ye, B., Han, S., Chen, H."Silencing of lncRNA TFAP2A‑AS1 attenuates the development of acute coronary syndrome by inhibiting TFAP2A expression". Biomedical Reports 24, no. 2 (2026): 20. https://doi.org/10.3892/br.2025.2093
Copy and paste a formatted citation
x
Spandidos Publications style
Huang S, Guan F, Ye F, Ye B, Han S and Chen H: Silencing of lncRNA TFAP2A‑AS1 attenuates the development of acute coronary syndrome by inhibiting TFAP2A expression. Biomed Rep 24: 20, 2026.
APA
Huang, S., Guan, F., Ye, F., Ye, B., Han, S., & Chen, H. (2026). Silencing of lncRNA TFAP2A‑AS1 attenuates the development of acute coronary syndrome by inhibiting TFAP2A expression. Biomedical Reports, 24, 20. https://doi.org/10.3892/br.2025.2093
MLA
Huang, S., Guan, F., Ye, F., Ye, B., Han, S., Chen, H."Silencing of lncRNA TFAP2A‑AS1 attenuates the development of acute coronary syndrome by inhibiting TFAP2A expression". Biomedical Reports 24.2 (2026): 20.
Chicago
Huang, S., Guan, F., Ye, F., Ye, B., Han, S., Chen, H."Silencing of lncRNA TFAP2A‑AS1 attenuates the development of acute coronary syndrome by inhibiting TFAP2A expression". Biomedical Reports 24, no. 2 (2026): 20. https://doi.org/10.3892/br.2025.2093
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