由FUBP1介导的调控RNA网络驱动三阴性乳腺癌细胞的增殖和侵袭。
Regulatory RNA network mediated by FUBP1 drives the proliferation and invasion of triple-negative breast cancer cells.
作者信息
Liu Wei, Liang Peide, Chen Lihong, Liang Rong, Xiong Xifeng
机构信息
Department of Breast Surgery, Guangzhou Red Cross Hospital of Jinan University, Guangzhou, 510220, Guangdong, China.
Department of Thyroid and Breast Surgery, Dongguan Hospital of Guangzhou University of Chinese Medicine, Dongguan, 523000, Guangdong, China.
出版信息
Med Oncol. 2025 Jun 28;42(8):293. doi: 10.1007/s12032-025-02871-6.
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.
我们早期的研究确定FUBP1是三阴性乳腺癌（TNBC）一个很有前景的生物标志物。然而，其在调控TNBC细胞增殖和侵袭的RNA网络中的作用仍不清楚。在此，我们构建了一个FUBP1表达降低的稳定MDA-MB-231细胞系，并进行了转录组测序。我们发现FUBP1敲低后有1084个差异表达的mRNA、2394个lncRNA和497个circRNA。KEGG分析显示PI3K-Akt信号传导和ECM受体相互作用等通路富集。值得注意的是，FUBP1敲低后lnc-CCNB1IP1-1-1下调，其抑制作用抑制了细胞增殖、迁移和侵袭。此外，lnc-CCNB1IP1-1-1敲低降低了PARP2的表达。因此，FUBP1敲低激活lnc-CCNB1IP1-1-1来调节TNBC进展，揭示了FUBP1在TNBC RNA网络中作用的新见解。
Zotero 插件