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Cancer/testis antigen  MAGEC 2, a member of the type I melanoma‐associated antigen family, is expressed in a wide variety of cancer types but not in normal somatic cells.  MAGEC 2 has long been recognized as a tumor‐specific target, however, its functions remain largely unknown. In this study, we established  MAGEC 2‐knockout A375 melanoma cell lines using the  CRISPR /Cas9 system. Seven clonal cell lines were generated by using four single guide  RNA s targeting the coding region of the   MAGEC 2  gene, which produced indels that abolished  MAGEC 2 protein expression. To identify the differentially expressed protein profiles associated with  MAGEC 2 loss, isobaric tag for relative quantitation‐based comparative proteomics experiments were carried out on the  MAGEC 2‐knockcout and control A375 cells. Mining of the proteomics data identified a total 224 (61.6% upregulated and 38.4% downregulated) proteins to be significantly altered in expression level in  MAGEC 2‐knockcout cells. Ingenuity Pathway Analysis indicated that the significantly altered proteins were involved in critical neoplasia‐related biological functions such as cell death, proliferation, and movement. Gene ontology analysis identified “apoptosis signaling” as the top‐most upregulated pathway associated with  MAGEC 2 loss. We showed that knockout or knockdown of the   MAGEC 2  gene sensitized melanoma cells to tumor necrosis factor‐α‐induced apoptosis. Interestingly, actin‐based motility by Rho and RhoA signaling, known to promote cell migration, were also identified as the top downregulated pathways in  MAGEC 2‐knockout A375 cells. In short, our study provides a suitable cell model for exploring the biological functions of  MAGEC 2 in malignant cells, and sheds light on the molecular pathway by which  MAGEC 2 promotes tumor development.

Establishment of MAGEC 2‐knockout cells and functional investigation of MAGEC 2 in tumor cells