Xu Wenbin, Yao Han, Wu Zhen, Yan Xiaojun, Jiao Zishan, Liu Yajing, Zhang Meng, Wang Donglai
State Key Laboratory of Common Mechanism Research for Major Diseases & Department of Medical Genetics, Institute of Basic Medical Sciences & School of Basic Medicine, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, 100005, China.
Nat Commun. 2024 Feb 14;15(1):1362. doi: 10.1038/s41467-024-45585-5.
Metastasis is the major cause of lung cancer-related death, but the mechanisms governing lung tumor metastasis remain incompletely elucidated. SE translocation (SET) is overexpressed in lung tumors and correlates with unfavorable prognosis. Here we uncover SET-associated transcription factor, zinc finger and BTB domain-containing protein 11 (ZBTB11), as a prometastatic regulator in lung tumors. SET interacts and collaborates with ZBTB11 to promote lung cancer cell migration and invasion, primarily through SET-ZBTB11 complex-mediated transcriptional activation of matrix metalloproteinase-9 (MMP9). Additionally, by transcriptional repression of proline-rich Gla protein 2 (PRRG2), ZBTB11 links Yes-associated protein 1 (YAP1) activation to drive lung tumor metastasis independently of SET-ZBTB11 complex. Loss of ZBTB11 suppresses distal metastasis in a lung tumor mouse model. Overexpression of ZBTB11 is recapitulated in human metastatic lung tumors and correlates with diminished survival. Our study demonstrates ZBTB11 as a key metastatic regulator and reveals diverse mechanisms by which ZBTB11 modulates lung tumor metastasis.
转移是肺癌相关死亡的主要原因,但肺肿瘤转移的调控机制仍未完全阐明。SET易位蛋白(SET)在肺肿瘤中过度表达,且与不良预后相关。在此,我们发现SET相关转录因子、含锌指和BTB结构域蛋白11(ZBTB11)是肺肿瘤中的促转移调节因子。SET与ZBTB11相互作用并协同促进肺癌细胞迁移和侵袭,主要通过SET-ZBTB11复合物介导的基质金属蛋白酶9(MMP9)转录激活。此外,通过对富含脯氨酸的Gla蛋白2(PRRG2)的转录抑制,ZBTB11将Yes相关蛋白1(YAP1)激活联系起来,独立于SET-ZBTB11复合物驱动肺肿瘤转移。ZBTB11缺失抑制肺肿瘤小鼠模型中的远处转移。ZBTB11的过表达在人类转移性肺肿瘤中重现,且与生存率降低相关。我们的研究证明ZBTB11是关键的转移调节因子,并揭示了ZBTB11调节肺肿瘤转移的多种机制。