Abstract
Gastric carcinoma (GC) is a malignant tumor, which is an important cause of death in all tumor deaths. The role of MARCH1 in GC has not been studied, this study aims to investigate the function of MARCH1 in GC. The expression of MARCH1 in normal tissue and tumor tissue was analyzed by TCGA-based GEPIA platform and UALCAL website and verified by RT-qPCR, Western blotting (WB), and Immunohistochemistry (IHC); CCK8 assay and crystal violet assay were separately used to detect cell viability and cell cloning ability. Cell spheroidization assay and Fluorescence-activated cell sorting (FACS) were performed to determine CD44+, CD133+ cell numbers to study the stemness characteristics of GC cells. While, WB was used to study the specific signaling pathway regulated by MARCH1. Animal model of GC was established to study the regulation of MARCH1 on GC growth in vivo. It showed that the expression of MARCH1 in GC tissues was higher than that in normal tissues; CCK8 and crystal violet assay showed that MARCH1 could promote cell viability and cloning ability of GC cells; cell spheroidization experiments and FACS showed that MARCH1 promoted the cloning ability of GC cells; WB results revealed that MARCH1 mainly regulated GC through the Wnt/β-catenin signaling pathway; In-vivo results showed that MARCH1 can promote the growth of GC. This study found that MARCH1 maintained the stemness characteristics and promoted the proliferation of GC cells by activating the Wnt/β-catenin signaling pathway.