Wu Song, Lu Jibu, Zhu Hongbo, Wu Feiyue, Mo Yunxian, Xie Liming, Song Cailu, Liu Lingrui, Xie Xiaoming, Li Yuehua, Lin Huan, Tang Hailin
State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat-Sen University Cancer Center, Guangzhou, China.
The First Affiliated Hospital of Hengyang Medical School, University of South China, Hengyang, China.
Cancer Lett. 2024 Jan 28;581:216508. doi: 10.1016/j.canlet.2023.216508. Epub 2023 Nov 28.
Among patients with triple-negative breast cancer (TNBC), distant metastasis is the leading cause of death. Our previous studies have shown that TNBC progression is greatly facilitated by circKIF4A, but uncertainty remains regarding its role in TNBC brain metastasis and the molecular mechanism. In this study, we found notable upregulation of circKIF4A in TNBC cell lines and brain metastases. Inhibition of circKIF4A impaired the ability of TNBC to proliferate, migrate, and cause brain metastasis. Luciferase reporter assays confirmed that circKIF4A competed for binding to miR-637 with STAT3 3' UTR. Western blot analysis revealed that inhibition of circKIF4A decreased STAT3 and p62 expression, while increased the LC3B-II/LC3B-I ratio and the expression of Beclin, indicating that downregulation of circKIF4A induced autophagy by competing with STAT3 for binding to miR-637. By employing a competitive endogenous RNA (ceRNA) mechanism, the circKIF4A-miR-637-STAT3 axis coordinates brain metastasis in TNBC. circKIF4A can therefore be used as a prognostic biomarker for brain metastasis in TNBC and as a therapeutic target.
在三阴性乳腺癌(TNBC)患者中,远处转移是主要的死亡原因。我们之前的研究表明,circKIF4A极大地促进了TNBC的进展,但其在TNBC脑转移中的作用及分子机制仍不明确。在本研究中,我们发现circKIF4A在TNBC细胞系和脑转移灶中显著上调。抑制circKIF4A会损害TNBC的增殖、迁移及导致脑转移的能力。荧光素酶报告基因检测证实,circKIF4A与STAT3 3' UTR竞争结合miR-637。蛋白质免疫印迹分析显示,抑制circKIF4A会降低STAT3和p62的表达,同时增加LC3B-II/LC3B-I比值及Beclin的表达,表明circKIF4A下调通过与STAT3竞争结合miR-637诱导自噬。通过竞争性内源RNA(ceRNA)机制,circKIF4A-miR-637-STAT3轴协同调控TNBC的脑转移。因此,circKIF4A可作为TNBC脑转移的预后生物标志物及治疗靶点。