Overexpression of N-acetylglucosaminyltransferase V promotes human parotid gland acinar cell immortalization via the epidermal receptor activation.
Ching-Chia ChengChih-Feng LinYong-Chong LinTai-Horng YoungPei-Jen LouPublished in: Journal of cellular physiology (2021)
The purpose of this study is to maintain the proliferation capability of human parotid gland acinar cells (ACs) in vitro to extend passage number and to study the mechanism that regulates AC stemness. N-acetylglucosaminyltransferase V (GnT-V) is the Golgi enzyme, and it has been reported that the β1,6GlcNAc-branched N-linked glycans are associated with various cell behaviors. Therefore, we modify the gene expression of ACs by transfection of the GnT-V-overexpression plasmid, and we found that upregulation of GnT-V extensively increased ACs proliferation and stemness properties in ACs/GnT-V compared to ACs transfected with Mock plasmid. More importantly, we observed that high levels of GnT-V positively correlated with ALDH1A3 expression via increasing phosphorylation of cell surface receptors and activating the downstream signaling transduction. Hence, the current study suggested that GnT-V is a significant factor for cell immortalization in the ACs model by activating the EGFR/ERK/ALDH1A3 signaling pathway.
Keyphrases
- signaling pathway
- acute coronary syndrome
- gene expression
- induced apoptosis
- cell proliferation
- endothelial cells
- single cell
- pi k akt
- epithelial mesenchymal transition
- stem cells
- escherichia coli
- small cell lung cancer
- cell surface
- cell therapy
- poor prognosis
- multidrug resistant
- crispr cas
- transcription factor
- cell cycle arrest
- protein kinase
- epidermal growth factor receptor
- endoplasmic reticulum stress
- cancer stem cells