Suppressing the MLK3 promotes glutamine metabolism: mechanism and implications in progression of colon cancer

This study was designed to explore the potential role of mixed-lineage protein kinase 3 (MLK3) in colorectal cancer (CRC) progression and its relationship with glutamine metabolism. The immunohistochemical staining results MLK3 were primarily collected through 100 CRC patients. Wound healing transwell assays used detect migration ability cells by transfecting siMlk3. Gene set variation analysis (GSVA) Spearman’s rank correlation coefficient as bioinformatics tools signaling pathways related MLK3. Western blotting performed analyze downstream suggested an increased expression tissues, which adverse clinicopathological characteristics those Knockdown inhibited proliferative migratory CRCs. Bioinformatics confirmed between malignancy pathways. cell lines transfected siMlk3 suppressed metabolism downregulating transporter alanine-serine-cysteine 2 (ASCT2). These vital progression, may be suppression transporter, namely alanine, serine, cysteine