SLC11A2(DMT1)-deletion RNA sequencing
Title: SLC11A2 act as a Driver of EMT and Tumorigenesis in Colon Adenocarcinoma. Abstract: The present study aimed to investigate the role of SLC11A2, a divalent metal transporter involved in iron metabolism, in the progression of colon adenocarcinoma (COAD). Bioinformatics analyses based on the The Cancer Genome Atlas, CPTAC and GEPIA2 databases were performed to evaluate SLC11A2 expression, and its association with patient survival and immune cell infiltration. CRISPR-mediated knockdown of SLC11A2 was carried out in SW480 and HCT116 cells. Cell viability, migration and invasion were subsequently assessed using Cell Counting Kit-8, wound healing and Transwell assays, respectively. In addition, xenograft mouse models were established to examine tumor growth and epithelial-mesenchymal transition (EMT) markers via immunohistochemistry. Results of the present study demonstrated that SLC11A2 expression was significantly upregulated in COAD tissues and was associated with poorer overall survival. SLC11A2 knockdown did not markedly affect cell viability; however, knockdown of this protein significantly suppressed cell migration and invasion. In vivo, SLC11A2 knockdown effectively inhibited tumor growth and attenuated EMT, as evidenced by increased E-cadherin expression and decreased expression of vimentin and N-cadherin. Collectively, these findings indicated that SLC11A2 promotes COAD progression through enhancing the migratory and invasive capacities of cancer cells, and facilitating EMT.