Abstract
Tensin 4 (TNS4) is overexpressed in multiple cancers, including colorectal cancer (CRC), and is associated with a poor prognosis of patients with CRC. However, the role and underlying mechanisms of TNS4 in CRC have yet to be elucidated. The expression of TNS4 in CRC tissues were analyzed by immunohistochemistry. Cell migration and invasion were assessed in vitro using Transwell assay. Western blot and reverse transcription (RT)-quantitative (q)PCR were used to investigate the molecular mechanisms by which TNS4 regulates aerobic glycolysis, migration and invasion of CRC cells. The present study demonstrated that TNS4 was highly expressed in the cancer tissues of patients with CRC and significantly associated with the tumor-node-metastasis stages. TNS4 silencing led to a significant decrease in glucose consumption and lactate production in CRC cells, and knockdown of TNS4 suppressed the migration and invasion of CRC cells via aerobic glycolysis through the β-catenin/c-Myc pathway. Notably, treatment with DASA-58, an activator of glycolysis, or SKL2001, an activator of β-catenin/c-Myc signaling, significantly reversed the effect of TNS4 knockdown on aerobic glycolysis, migration and invasion of CRC cells. Collectively, these results suggest that TNS4 may act as a novel regulator of aerobic glycolysis, migration and invasion of CRC cells by modulating β-catenin/c-Myc signaling, providing a new potential biomarker and therapeutic target in CRC.