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B4GALNT1 promotes progression and metastasis in lung adenocarcinoma through JNK/c-Jun/Slug pathway
被引:15
|作者:
Jiang, Tian
[1
]
Wu, Hao
[2
,3
]
Lin, Miao
[1
]
Yin, Jun
[1
]
Tan, Lijie
[1
]
Ruan, Yuanyuan
[2
]
Feng, Mingxiang
[1
]
机构:
[1] Fudan Univ, Zhongshan Hosp, Dept Thorac Surg, 180 Fenglin Rd, Shanghai 200032, Peoples R China
[2] Fudan Univ, Sch Basic Med Sci, Dept Biochem & Mol Biol, 138 Yixueyuan Rd, Shanghai 200032, Peoples R China
[3] Fudan Univ, Zhongshan Hosp, Dept Clin Lab Med, Shanghai, Peoples R China
基金:
中国国家自然科学基金;
关键词:
CANCER STEM-CELLS;
GROWTH;
GM2;
EXPRESSION;
SYNTHASE;
BIOSYNTHESIS;
APOPTOSIS;
MIGRATION;
MOTILITY;
ANTIBODY;
D O I:
10.1093/carcin/bgaa141
中图分类号:
R73 [肿瘤学];
学科分类号:
100214 ;
摘要:
Lung adenocarcinoma (LUAD) is one of the most common types of cancer and has a low survival rate. beta-1,4-N-Acetyl galactosaminyltransferase 1 (B4GALNT1), which is involved in the synthesis of complex gangliosides, is highly expressed in the progression of various cancers. This study aimed to elucidate the biological functions of B4GALNT1 in LUAD progression and metastasis. We observed that B4GALNT1 overexpression showed enhanced cell migration and invasion in vitro, and promoted tumor metastasis, with reduced survival in mice. Mechanistically, B4GALNT1 regulated metastatic potential of LUAD through activating the JNK/c-Jun/Slug pathway, and with the form of its enzymatic activity. Clinical samples confirmed that B4GALNT1 expression was upregulated in LUAD, and B4GALNT1 was correlated with c-Jun/Slug expression, lymph node involvement, advanced clinical stage, and reduced overall survival. Collectively, our results suggest that B4GALNT1 promotes progression and metastasis of LUAD through activating JNK/c-Jun/Slug signaling, and with the form of its enzymatic activity.
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页码:621 / 630
页数:10
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