| First Author | Han F | Year | 2018 |
| Journal | EBioMedicine | Volume | 31 |
| Pages | 253-266 | PubMed ID | 29739711 |
| Mgi Jnum | J:275038 | Mgi Id | MGI:6296172 |
| Doi | 10.1016/j.ebiom.2018.04.026 | Citation | Han F, et al. (2018) SOX30 Inhibits Tumor Metastasis through Attenuating Wnt-Signaling via Transcriptional and Posttranslational Regulation of beta-Catenin in Lung Cancer. EBioMedicine 31:253-266 |
| abstractText | Although high mortality of lung cancer is greatly due to distant metastasis, the mechanism of this metastasis remains unclear. Here, we investigate in lung cancer that SOX30 is sharply under-expressed in metastatic tumors compared with non-metastatic tumors, and suppresses plenty of metastasis related processes or pathways. SOX30 strongly inhibits tumor cell metastasis in vitro and in vivo. Sox30 deficiency promotes lung metastasis in Sox30(-/-) mice and this uncontrollable lung-metastasis is re-inhibited upon Sox30 re-expression. Mechanistically, SOX30 diminishes Wnt-signaling via directly transcriptional repressing beta-catenin or interacting with beta-catenin to compete with TCF for binding to beta-catenin. The carboxyl-terminus of SOX30 is required for attenuating beta-catenin transcriptional activity, whereas the amino-terminus of SOX30 is required for its interaction with beta-catenin protein. Enhance of beta-catenin attenuates the anti-metastatic role of SOX30. Moreover, Sox30 deficiency promotes tumor metastasis and reduces survival of mice. In addition, nuclear SOX30 expression is closely associated with metastasis and represents a favorable independent prognostic biomarker of lung cancer patients. Altogether, these results highlight an important role and mechanism of SOX30 in lung cancer metastasis, providing a potential therapeutic target for anti-metastasis. |
