J Cancer 2019; 10(25):6286-6297. doi:10.7150/jca.33765 This issue

Research Paper

Galectin-1 Promotes Vasculogenic Mimicry in Gastric Cancer by Upregulating EMT Signaling

Xiaolan You, Qinghong Liu, Jian Wu, Yuanjie Wang, Jiawen Dai, Dehu Chen, Yan Zhou, Yanjun Lian

Department of Gastrointestinal Surgery, Hospital Affiliated 5 to Nantong University (Taizhou People's Hospital), Taizhou, Jiangsu province, China

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You X, Liu Q, Wu J, Wang Y, Dai J, Chen D, Zhou Y, Lian Y. Galectin-1 Promotes Vasculogenic Mimicry in Gastric Cancer by Upregulating EMT Signaling. J Cancer 2019; 10(25):6286-6297. doi:10.7150/jca.33765. Available from https://www.jcancer.org/v10p6286.htm

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Background: Galectin-1 (Gal-1) expression was positively associated with vasculogenic mimicry (VM) in primary gastric cancer (GC) tissue, and that both Gal-1 expression and VM in GC tissue are indicators of poor prognosis. However, whether Gal-1 promotes VM, and by what mechanismsremains unknown.

Methods: To investigate the underlying mechanisms,wound healing assay, proliferation assay, invasion assay, and three-dimensional culture were used to evaluate the invasion, metastasis and promoted VM formation effects of the Gal-1. We monitored the expression level of sociated proteins in GC tissues, cell lines in vitro and nude mice tumorigenicity in vivo by immunohistochemistry and western blot.

Results: Gal-1 overexpression significantly promoted the proliferation, invasion, migration, and VM formation of MGC-803 cells. Gal-1 was associated with E-cadherin and vimentin in vitro and in clinical samples. The epithelial-to-mesenchymal transition (EMT) induced in MGC-803 cells by TGF-β1 was accompanied by Gal-1 activation and promotion of VM formation, while knockdown of Gal-1 reduced the response to TGF-β1, suggesting that Gal-1 promotes VM formation by activating EMT signaling. Overexpression of Gal-1 accelerated subcutaneous xenograft growth and facilitated pulmonary metastasis in athymic mice, enhanced the expression of EMT markers, and promoted VM formation in vivo.

Conclusion: Our results indicated that Gal-1 promotes VM in GC by upregulating EMT signaling; thus, Gal-1 and this pathway are potential novel targets to treat VM in GC.

Keywords: Galectin-1, Vasculogenic mimicry, Gastric cancer, Epithelial-to-mesenchymal transition