LGR4减弱骨钙素（MGP）表达并抑制表皮生长因子受体（EGFR）激活诱导的三阴性乳腺癌转移。
LGR4 attenuates MGP expression and suppresses EGFR activation-induced triple-negative breast cancer metastasis.
作者信息
Li Qishuang, Gao Yankun, Huo Zitian, Liu Jing, Zhang Pumin, Wang Yi
机构信息
State Key Laboratory of Targeting Oncology, National Center for International Research of Biotargeting Theranostics, Guangxi Key Laboratory of Biotargeting Theranostics, Collaborative Innovation Center for Targeting Tumor Diagnosis and Therapy, Guangxi Medical University Nanning 530021, Guangxi, PR China.
State Key Laboratory of Proteomics, Beijing Proteome Research Center, National Center for Protein Sciences (Beijing), Beijing Institute of Lifeomics Beijing 102206, PR China.
出版信息
Am J Cancer Res. 2024 Jul 15;14(7):3419-3432. doi: 10.62347/THII9650. eCollection 2024.
Breast cancer has emerged as the most common cancer globally, with a significant reduction in overall survival rate after metastasis. Compared with other types of breast cancer, triple-negative breast cancer (TNBC) is more prone to metastasize, presenting substantial treatment challenges due to the lack of effective therapies. LGR4, which is highly expressed in breast cancer, has been shown to promote the proliferation and invasion of breast cancer cells. However, its specific role in TNBC remains unclear. In this study, we applied a multi-omics approach to explore the regulatory mechanism of LGR4 in TNBC metastasis. Our findings showed that LGR4 could regulate actin cytoskeletal through EGFR and curtail EGFR activation-induced TNBC metastasis by inhibiting MGP expression. These insights provide new perspectives on the role of LGR4 in breast cancer metastasis.
乳腺癌已成为全球最常见的癌症，转移后总体生存率显著降低。与其他类型的乳腺癌相比，三阴性乳腺癌（TNBC）更容易发生转移，由于缺乏有效的治疗方法，带来了巨大的治疗挑战。LGR4在乳腺癌中高表达，已被证明可促进乳腺癌细胞的增殖和侵袭。然而，其在TNBC中的具体作用仍不清楚。在本研究中，我们应用多组学方法探讨LGR4在TNBC转移中的调控机制。我们的研究结果表明，LGR4可通过EGFR调节肌动蛋白细胞骨架，并通过抑制MGP表达减少EGFR激活诱导的TNBC转移。这些见解为LGR4在乳腺癌转移中的作用提供了新的视角。
Zotero 插件