B4GALNT1 enhances cell proliferation and growth in oral squamous cell carcinoma via p38 and JNK MAPK pathway

• Published in: Translational cancer research Vol. 9; no. 4; pp. 2340 - 2348
• Main Authors: Jing, Shaohong, Deng, Zhaoming, Liang, Lizhong, Liang, Jun
• Format: Journal Article
• Language: English
• Published: China AME Publishing Company 01.04.2020
• Subjects: Original; MAPK pathway; cell growth; oral squamous cell carcinoma (OSCC); cell proliferation; Beta-1,4-N-Acetyl-Galactosaminyltransferase 1 (B4GALNT1)
• ISSN: 2218-676X; 2219-6803
• DOI: 10.21037/tcr.2020.03.73

Beta-1,4-N-Acetyl-Galactosaminyltransferase 1 (B4GALNT1) was reported to play an important role in the development of the central nervous systems. We found higher expression of B4GALNT1 in oral squamous cell carcinoma (OSCC) tissues compared to the paired normal adjacent tissues in the TCGA database. This study aimed to investigate whether there was a potential relationship between B4GALNT1 and OSCC tumorigenesis and further explored the possible regulation mechanism. Gene expression level was analyzed by means of real-time quantitative PCR and further cell function experiments were performed including cell proliferation and apoptosis test, cell cycle distribution detection after silencing B4GALNT1 by transfection with B4GALNT1-shRNA lentivirus. Western Blotting was carried out to explore the possible molecular mechanism. The present study confirmed the overexpression of B4GALNT1 in OSCC. Compared to the control group, cell proliferation after silencing B4GALNT1 was significantly inhibited and cell apoptosis percentage was significantly higher. Besides, the knockdown of B4GALNT1 resulted in cell cycle arrest at G1 phase in our experiment. B4GALNT1 enhances the proliferation and suppress the apoptosis of OSCC cells probably through JNK and p38 signaling pathway.