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

Abstract

Background 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. Methods 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. Results 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. Conclusions B4GALNT1 enhances the proliferation and suppress the apoptosis of OSCC cells probably through JNK and p38 signaling pathway.

Androgen receptor variant 7 exacerbates hepatocarcinogenesis in a c-MYC-driven mouse HCC model

“…The B4galnt1 gene encodes the enzyme beta-1,4-N-acetylgalactosaminyl transferase, involved in the biosynthesis of complex gangliosides. Various studies demonstrated that B4GALNT1 was involved in the progression of different cancer types including oral squamous cell carcinoma and lung adenocarcinoma [ 32 , 33 ]. Quantitative RT-PCR analysis showed that it was upregulated by c-MYC but was further elevated by AR-V7 co-expression in both male and female HCC samples (Fig.…”

Network pharmacology and experiment validation investigate the potential mechanism of triptolide in oral squamous cell carcinoma

“…Chen et al also demonstrated that triptolide can induce apoptosis of OSCC cell lines SCC-25 and OEC-M1 in vivo by activating caspase-25 and caspase-1 ( Chen et al, 2009 ). The downregulation of B4GALNT1 can inhibit proliferation and growth in OSCC cells via the JNK pathway ( Jing et al, 2020 ). Curcumin analogue HO-3867 affects cell growth in OSCC cells by triggering activated cysteine protease and PARP through the JNK1/2 pathway ( Chen et al, 2022 ).…”

“…JAK2/ STAT3 signaling activates epiregulin-induced cancerassociated fibroblasts, which stimulates the epithelial-mesenchymal transition (EMT) of OSCC cells, which is necessary for migration and invasion (Wang et al, 2019). CCL18 promotes cell growth, metastasis, and EMT in OSCC through the JAK2/STAT3 signaling pathway (Jiang et al, 2020). Inhibition of HNF1A-SA1 expression suppresses the proliferation, migration, and EMT of OSCC cells through the Notch signaling pathway, whereas STAT3 promotes HNF1A-SA1 upregulation (Liu et al, 2019).…”

Machine Learning-Based Identification of B4GALNT1 as a Key Player in Hepatocellular Carcinoma: A Comprehensive Bioinformatics and Structural Analysis

“…The change in expression or mutation B4GALNT1 has been associated with tumor progression in melanoma [9] by inducing of gangliosides GM2/GD2, clear cell renal cell carcinoma (ccRCC) [10], colorectal cancer [11], lung adenocarcinoma [12], oral squamous cell carcinoma [13], breast cancer [14] and cervical cancer [15]. Apart from cancer B4GALNT1 has been associated with Hereditary Spastic Paraplegia [16], Parkinson’s disease [17] and Axonal Charcot-Marie-Tooth Disease [18].…”