Background
Bitter taste receptor 14 belongs (TAS2R14) to GPCR family, stimulated by epigallocatechin gallate (EGCG). We reported the EGCG administration induced downregulation of histamine receptors in oral epithelial cancer cell lines. It is reported that usage of histamine receptor antagonists inhibited cancer cell metastasis through suppressing epithelial to mesenchymal transition (EMT). The current study investigates the function of TAS2R14 for histamine receptors and EMT.
Method
We performed knock out of TAS2R14 in HSC4 oral epithelial cancer cell line by genome editing method. The cultured cells extractions were prepared for the western blot analysis. Histamine H1 and H2 receptor antibodies were used for detection of protein expression. For the biochemical analysis of EMT, E-cadherin and N-cadherin antibodies were used.
Results
Genome editing of TAS2R14 in three HSC4 cells resulted in integration of pretermination codon in the gene. TAS2R14 protein in edited HSC4 cells was not detected by western blot analysis. E-cadherin was upregulated and N-cadherin was down regulated. Furthermore, histamine H1 and H2 receptors were down regulated.
Conclusions and discussion
TAS2R14 is involved in regulation of EMT marker proteins and histamine H1 and H2 receptors expression. EGCG administration to HSC4 cells means that there might be other molecular targets of EGCG or EGCG might function as inverse agonist considering the reports that bitter taste receptors work as constitutive active receptors.