Solute carrier family 35 member D3 promotes colorectal cancer progression through AMPK signaling pathway

Abstract

AbstractThis article is aim to investigate the functional role and potential regulatory mechanisms of solute carrier family 35 member D3 (SLC35D3) in colorectal cancer. Beyond analyzing databases, western blot was used to detect and verify the expression of SLC35D3. Cell proliferation and invasion or migration ability were detected by CCK‐8, EdU, and Transwell assays. Animal experiments were conducted to verify if the biological function of SLC35D3 in vivo is consistent with that in vitro. Beyond SLC family pathway enrichment analysis, the relationship between SLC35D3 and metabolic pathway AMPK was explored using co‐immunoprecipitation and western blot. SLC35D3 is highly expressed in colorectal cancer (CRC) tissue. The overexpression or down regulation of SLC35D3 has been shown to promote or inhibit the biological functions of colorectal cancer, and similar experimental results can be verified in vivo experiments. Based on the high correlation between the SLC family and metabolic pathways, we chose the metabolic‐related AMPK pathway as the subject of our research. Co‐immunoprecipitation and protein analysis demonstrated that SLC35D3 may bind to AMPK molecules and regulate the AMPK pathway of colorectal cancer cells. Based on the above facts, SLC35D3 promotes colorectal cancer progression through regulating AMPK signaling pathway.