2. Academic Validation
  3. B4GALNT1 promotes progression and metastasis in lung adenocarcinoma through JNK/c-Jun/Slug pathway

B4GALNT1 promotes progression and metastasis in lung adenocarcinoma through JNK/c-Jun/Slug pathway

  • Carcinogenesis. 2021 Apr 30;42(4):621-630. doi: 10.1093/carcin/bgaa141.
Tian Jiang 1,  Hao Wu 2 3,  Miao Lin 1,  Jun Yin 1,  Lijie Tan 1,  Yuanyuan Ruan 2,  Mingxiang Feng 1
Affiliations

Affiliations

  • 1 Department of Thoracic Surgery, Zhongshan Hospital, Fudan University, No.180 Fenglin Road, Shanghai, China.
  • 2 Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Fudan University, Shanghai, China.
  • 3 Department of Clinical Laboratory Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.
PMID: 33367717 DOI: 10.1093/carcin/bgaa141
Abstract

Lung adenocarcinoma (LUAD) is one of the most common types of Cancer and has a low survival rate. β-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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