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<p>Our earlier research identified FUBP1 as a promising biomarker for triple-negative breast cancer (TNBC). However, its role in RNA networks governing TNBC cell proliferation and invasion remains unclear. Here, we developed a stable MDA-MB-231 cell line with reduced FUBP1 expression and performed transcriptome sequencing. We found 1084 differentially expressed mRNAs, 2394 lncRNAs, and 497 circRNAs following FUBP1 knockdown. KEGG analysis showed enrichment in pathways like PI3K-Akt signaling and ECM receptor interaction. Notably, lnc-CCNB1IP1-1-1 was down-regulated upon FUBP1 knockdown, and its suppression inhibited cell proliferation, migration, and invasion. Additionally, lnc-CCNB1IP1-1-1 knockdown reduced PARP2 expression. Thus, FUBP1 knockdown activates lnc-CCNB1IP1-1-1 to modulate TNBC progression, revealing new insights into FUBP1’s role in TNBC RNA networks.</p>

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Regulatory RNA network mediated by FUBP1 drives the proliferation and invasion of triple-negative breast cancer cells

  • 期刊论文

  • 发表日期：

    2025年6月28日

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  • Wei Liu,
  • Peide Liang,
  • Lihong Chen,
  • Rong Liang,
  • Xifeng Xiong

摘要

Our earlier research identified FUBP1 as a promising biomarker for triple-negative breast cancer (TNBC). However, its role in RNA networks governing TNBC cell proliferation and invasion remains unclear. Here, we developed a stable MDA-MB-231 cell line with reduced FUBP1 expression and performed transcriptome sequencing. We found 1084 differentially expressed mRNAs, 2394 lncRNAs, and 497 circRNAs following FUBP1 knockdown. KEGG analysis showed enrichment in pathways like PI3K-Akt signaling and ECM receptor interaction. Notably, lnc-CCNB1IP1-1-1 was down-regulated upon FUBP1 knockdown, and its suppression inhibited cell proliferation, migration, and invasion. Additionally, lnc-CCNB1IP1-1-1 knockdown reduced PARP2 expression. Thus, FUBP1 knockdown activates lnc-CCNB1IP1-1-1 to modulate TNBC progression, revealing new insights into FUBP1’s role in TNBC RNA networks.