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

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

doi:10.7150/jca.33765

International Journal of Biological Sciences

International Journal of Medical Sciences

Theranostics

Nanotheranostics

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

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

Citation:

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. https://www.jcancer.org/v10p6286.htm

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Abstract

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

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APA

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

ACS

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.

NLM

CSE

You X, Liu Q, Wu J, Wang Y, Dai J, Chen D, Zhou Y, Lian Y. 2019. Galectin-1 Promotes Vasculogenic Mimicry in Gastric Cancer by Upregulating EMT Signaling. J Cancer. 10(25):6286-6297.

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