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Updated: Dec 8, 2025

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
LncRNA AFAP1-AS1 Knockdown Represses Cell Proliferation, Migration, and Induced Apoptosis in Breast Cancer by
Bo Cai1, Xichao Wang1, Qing'ao Bu1
1Department of Thyroid Surgery & Ward Area of Breast Surgery, Shengli Oilfield Central Hospital, Dongying, China.
Abstract:
Long non-coding RNA actin filament-associated protein1-antisense RNA 1 (AFAP1-AS1) was confirmed to be associated with tumorigenesis. However, the role of AFAP1-AS1 in breast cancer was little known. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the levels of AFAP1-AS1, microRNA-497-5p (miR-497-5p), and Septin 2 (SEPT2) in breast cancer tissues and cells. The cell proliferation, migration, and apoptosis were tested by Methylthiazolyldiphenyl-tetrazolium bromide (MTT), Transwell and Flow cytometry assays, respectively. The targeting relationship between genes was predicted by StarBase v.3.0 and confirmed by dual-luciferase reporter assay. Pearson's correlation coefficient was applied to examine the correlation between the two groups. SEPT2 protein expression was evaluated by Western blot. Xenograft models were established to investigate the role of AFAP1-AS1 knockdown in vivo. AFAP1-AS1 was upregulated in breast cancer tissues and cells, and AFAP1-AS1 knockdown could hinder proliferation and migration of breast cancer cells, and contribute to cell apoptosis. MiR-497-5p, which was downregulated in breast cancer, was verified to be a target of AFAP1-AS1 and inversely correlated with AFAP1-AS1 expression. SEPT2, as a target gene of miR-497-5p, was negatively regulated by miR-497-5p and positively correlated with AFAP1-AS1 expression. Importantly, AFAP1-AS1 could upregulate SEPT2 expression by sponging miR-497-5p, and modulate cell progression by regulation of the miR-497-5p/SEPT2 axis in breast cancer. AFAP1-AS1 knockdown repressed the progression of breast cancer cells by sponging miR-497-5p and downregulating SEPT2.
Insights
Long non-coding RNA AFAP1-AS1 promotes breast cancer progression by upregulating SEPT2 via sponging miR-497-5p. Knocking down AFAP1-AS1 inhibits tumor growth, migration, and enhances apoptosis in breast cancer cells.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Long non-coding RNA actin filament-associated protein1-antisense RNA 1 (AFAP1-AS1) is implicated in tumorigenesis.
- The specific role of AFAP1-AS1 in breast cancer remains largely uncharacterized.
Purpose of the Study:
- To investigate the function of AFAP1-AS1 in breast cancer.
- To elucidate the molecular mechanism involving AFAP1-AS1, microRNA-497-5p (miR-497-5p), and Septin 2 (SEPT2) in breast cancer progression.
Main Methods:
- Quantitative real-time PCR (qRT-PCR) for gene expression analysis.
- Cell proliferation, migration, and apoptosis assays (MTT, Transwell, Flow cytometry).
- Dual-luciferase reporter assay, Western blot, and xenograft models for mechanistic and in vivo validation.
Main Results:
- AFAP1-AS1 was significantly upregulated in breast cancer tissues and cells.
- AFAP1-AS1 knockdown suppressed proliferation and migration, while promoting apoptosis.
- AFAP1-AS1 acts as a sponge for miR-497-5p, leading to upregulation of its target gene, SEPT2.
Conclusions:
- AFAP1-AS1 promotes breast cancer progression by regulating the miR-497-5p/SEPT2 axis.
- Targeting AFAP1-AS1 may represent a potential therapeutic strategy for breast cancer.
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