Scholarlink

<p>N6-methyladenosine (m6A), a key RNA epigenetic modification, plays a crucial role in regulating tumor malignancy. The mechanisms by which m6A regulates long noncoding RNA (lncRNA) in the malignant phenotype of epithelial–mesenchymal transition (EMT) require further exploration. This study combines bioinformatics analysis and cell experiments to investigate the role of m6A-regulated lncRNA in EMT. Bioinformatics data from The Cancer Genome Atlas database were analyzed. In vitro experiments established a stable overexpression cell line to investigate AC022509.1’s regulatory effect on the invasive and migratory phenotype of breast cancer. We employed RT-qPCR and western blot to investigate the regulatory impact of IGF2BP2 knockdown and overexpression on AC022509.1. We identified 481 lncRNAs that were co-expressed with m6A modifiers and EMT-related genes. Subsequent survival analysis identified 15 lncRNAs with prognostic significance. Utilizing the random forest method, AC022509.1 was determined to have the highest prognostic value among the identified lncRNAs. Analysis of transcriptomic and clinical data from patients with breast cancer reveals that AC022509.1 is under-expressed in breast cancer tissues, with higher expression levels associated with a favorable prognosis. A negative correlation was observed between lymph node metastases and AC022509.1 expression levels, which was further validated by clinical samples. Bioinformatics analyses indicate that AC022509.1 is linked to multiple tumor-related signaling pathways and negatively correlates with EMT scores. Experimental studies reveal that AC022509.1 overexpression reduces the invasiveness and migratory capabilities of MCF-7 and MDA-MB-231 cell lines. Furthermore, differential and correlation analyses reveal a significant association between AC022509.1 and the m6A regulatory factor IGF2BP2. Cell-based experiments show that IGF2BP2 regulates the expression level of AC022509.1. AC022509.1 functions as a tumor suppressor in breast cancer and is valuable as a prognostic marker and diagnostic target. Downregulation diminishes the invasive and migratory capabilities of breast cancer cells, with expression regulated by the m6A factor IGF2BP2.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Machine learning-based identification of m6A-regulated lncRNA AC022509.1 as a key modulator of EMT in breast cancer

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年7月28日

查看全文
  • Qinglan Wang,
  • Xianqiang Du,
  • Yanzhen Chen,
  • Rongrong Lin

摘要

N6-methyladenosine (m6A), a key RNA epigenetic modification, plays a crucial role in regulating tumor malignancy. The mechanisms by which m6A regulates long noncoding RNA (lncRNA) in the malignant phenotype of epithelial–mesenchymal transition (EMT) require further exploration. This study combines bioinformatics analysis and cell experiments to investigate the role of m6A-regulated lncRNA in EMT. Bioinformatics data from The Cancer Genome Atlas database were analyzed. In vitro experiments established a stable overexpression cell line to investigate AC022509.1’s regulatory effect on the invasive and migratory phenotype of breast cancer. We employed RT-qPCR and western blot to investigate the regulatory impact of IGF2BP2 knockdown and overexpression on AC022509.1. We identified 481 lncRNAs that were co-expressed with m6A modifiers and EMT-related genes. Subsequent survival analysis identified 15 lncRNAs with prognostic significance. Utilizing the random forest method, AC022509.1 was determined to have the highest prognostic value among the identified lncRNAs. Analysis of transcriptomic and clinical data from patients with breast cancer reveals that AC022509.1 is under-expressed in breast cancer tissues, with higher expression levels associated with a favorable prognosis. A negative correlation was observed between lymph node metastases and AC022509.1 expression levels, which was further validated by clinical samples. Bioinformatics analyses indicate that AC022509.1 is linked to multiple tumor-related signaling pathways and negatively correlates with EMT scores. Experimental studies reveal that AC022509.1 overexpression reduces the invasiveness and migratory capabilities of MCF-7 and MDA-MB-231 cell lines. Furthermore, differential and correlation analyses reveal a significant association between AC022509.1 and the m6A regulatory factor IGF2BP2. Cell-based experiments show that IGF2BP2 regulates the expression level of AC022509.1. AC022509.1 functions as a tumor suppressor in breast cancer and is valuable as a prognostic marker and diagnostic target. Downregulation diminishes the invasive and migratory capabilities of breast cancer cells, with expression regulated by the m6A factor IGF2BP2.