Ectopic expression of ERBB2/ERBB3 mutants upregulated PD-L1 expression in GBC cells, effectively suppressed normal T-cell-mediated cytotoxicity in vitro through activation of the PI3K/Akt signalling pathway and contributed to the growth and progression of GBC in vivo.
In conclusion, miR-143-3p suppresses tumour angiogenesis and growth of GBC through the ITGA6/PI3K/AKT/PLGF pathways and may be a novel molecular therapeutic target for GBC.
Consistent with STYK1 gene knockdown, AKT specific inhibitor MK2206 abrogated tumor promoting action induced by STYK1, suggesting that PI3K/AKT pathway is essential for the oncogenic role of STYK1 in GBC.
Frequent mutations were identified in tumor protein 53 (<i>TP53</i>) (14/27), SMAD family member 4 (<i>SMAD4</i>) (6/27), phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit α (<i>PIK3CA</i>) (6/27), and Kirsten rat sarcoma (<i>KRAS</i>) (6/27); no significant differences were identified between EBDC and GBC tissues.