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作者

Tianshu Miao Yilin Zhang Feng Tian Xiaoying Xu Qin Wei Xiaoyu Jiang Lijuan Ma Pengju Zhang Fengzhe Chen Xiaoyan Lin

作者单位

³Department of Pathology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, 250021, China ¹Key Laboratory Experimental Teratology of the Ministry of Education, Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, 250012, China ²These authors contributed equally. ⁵Lead contact ⁴Department of Infectious Disease, Central Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, 250013, China.

刊名

iScience

年份

2025

页码

113647

ISSN

2589-0042

摘要

Manic Fringe , a fucose-specific β-1,3-N-acetylglucosaminyltransferase, is critically involved in different cancers. However, the potential role and underlying mechanism of MFNG in the progression of lung adenocarcinoma remains unclear. Here, we found that MFNG was significantly down-regulated in LUAD tissues compared with adjacent non-cancerous tissues. Moreover, its decreased expression was associated with aggressive LUAD characteristics, including high grade and poor prognosis. Functional st...更多

Manic Fringe , a fucose-specific β-1,3-N-acetylglucosaminyltransferase, is critically involved in different cancers. However, the potential role and underlying mechanism of MFNG in the progression of lung adenocarcinoma remains unclear. Here, we found that MFNG was significantly down-regulated in LUAD tissues compared with adjacent non-cancerous tissues. Moreover, its decreased expression was associated with aggressive LUAD characteristics, including high grade and poor prognosis. Functional studies revealed that MFNG deficiency promoted migratory and invasive capabilities as well as epithelial-mesenchymal transition of LUAD cells in vitro and metastatic potential in vivo. Mechanistically, we found that MFNG silencing resulted in a remarkable activation of TGF-β/Smad signaling pathway. Pharmacological treatment with a TGF-β receptor kinase inhibitor alleviated the progressive phenotypes of LUAD cells induced by MFNG loss. Together, our results reveal a potential mechanism by which MFNG regulates LUAD progression and suggest that patients with advanced LUAD exhibiting MFNG deficiency may benefit from TGF-β signaling inhibition.收起

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