Knockdown of B3GNT3 inhibits colon cancer cell growth and migration

Abstract

Colon cancer (CC) ranks among the most common malignant tumors globally. Providing theoretical support is essential to controlling CC and improving patients’ prognoses. Beta-1,3-N-acetylglucosaminyltransferase 3 (B3GNT3), a protein-coding gene that encodes a member of the B3GNT family, affects multiple tumors. However, B3GNT3 remains largely unknown in terms of its role and mechanism in CC development and metastasis. This study explored B3GNT3’s effect on CC progression. We revealed that B3GNT3 is highly expressed in human CC tissues. B3GNT3 depletion suppressed CC cell growth. Knocking down B3GNT3 restrained CC cells’ motility. Mechanically, B3GNT3 knockdown blocks the nuclear factor kappa-B (NF-κB) pathway in CC cells. In summary, B3GNT3 depletion restrained CC cells’ growth and motility by targeting NF-κB pathway. As a potential target for CC, B3GNT3 appears promising.

Keywords

• colon cancer (cc)
• beta-1,3-n-acetylglucosaminyltransferase 3 (b3gnt3)
• growth
• motility
• nf-κb pathway