Research Papers:

SLC3A2, antigen of mAb 3G9, promotes migration and invasion by upregulating of mucins in gastric cancer

Shanshan Wang, Haibo Han, Ying Hu, Wei Yang, Yunwei Lv, Limin Wang, Lianhai Zhang and Jiafu Ji _

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Oncotarget. 2017; 8:88586-88598. https://doi.org/10.18632/oncotarget.19529

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Shanshan Wang1,*, Haibo Han2,*, Ying Hu2,*, Wei Yang1, Yunwei Lv1, Limin Wang1, Lianhai Zhang3 and Jiafu Ji3

1Department of Clinical Laboratory, Key laboratory of Carcinogenesis and Translational Research (Ministry of Education), Beijing, PR China

2Department of Biobank, Key laboratory of Carcinogenesis and Translational Research (Ministry of Education), Beijing, PR China

3Department of Gastrointestinal Surgery, Peking University Cancer Hospital and Institute, Beijing, PR China

*These authors contributed equally to this work

Correspondence to:

Jiafu Ji, email: [email protected]

Limin Wang, email: [email protected]

Lianhai Zhang, email: [email protected]

Keywords: gastric cancer, monoclonal antibody, SLC3A2, metastasis, invasion

Received: February 22, 2017     Accepted: April 17, 2017     Published: July 25, 2017


Solute carrier family 3 member 2 (SLC3A2) has been reported to be highly expressed in a variety of carcinomas. However, the function of SLC3A2 in gastric carcinoma (GC) has not been well explored. Monoclonal antibody (mAb) 3G9, generated from immunogen of various human GC cell lines, has been shown to bind to GC tissues specifically. In this study, we identified the target antigen of mAb 3G9 as SLC3A2, and detected the expression profile of SLC3A2 in a panel of gastric cancer cell lines and GC tumor tissues. We found that the increased expression of SLC3A2 was associated with serosal invasion in GC patients. Knockout of SLC3A2 suppressed the migration and invasion of BGC-823 cells in vitro and in vivo, whereas overexpression of SLC3A2 in NCI-N87 cells promoted the migration and invasion in vitro and in vivo. Mechanistic investigations suggested that MUC1, MUC16 and MUC5B were the downstream genes of SLC3A2 in GC cells. Taken together, our data suggested that SLC3A2 promoted the aggressive phenotype of GC by upregulating several mucin genes expression and may serve as a potential biomarker for diagnosis and target therapy.

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