The present study aimed to investigate whether microRNA (miR)-490-3p can regulate MAPK1 expression, increase proliferation of esophageal squamous cell carcinoma (ESCC) and reduce ESCC cell apoptosis.
Overexpression of miR-133b could suppress proliferation, migration and invasion of ESCC cells by inhibiting MAPK/ERK and PI3K/AKT signaling pathways through targeting EGFR, indicating that miR-133b might be a potential therapeutic target for the treatment of ESCC.
Ricolinostat (ACY-1215) suppresses proliferation and promotes apoptosis in esophageal squamous cell carcinoma via miR-30d/PI3K/AKT/mTOR and ERK pathways.
Down-regulation of RIP3 potentiates cisplatin chemoresistance by triggering HSP90-ERK pathway mediated DNA repair in esophageal squamous cell carcinoma.
Taken together, the current study was the first to demonstrate the upregulation of PD-L1 by chemotherapy in ESCC and its regulation through the EGFR/ERK pathway.
Importantly, we proved that RhoE could negatively regulate the protein expression of EGFR and p-ERK, suggesting that RhoE might inhibit ESCC progression through the EGFR/ERK pathway.
These data show that overexpression of Aurora-A contributes to the malignancy development of ESCC by enhancing tumor cell invasion as well as MMP-2 activity and expression, which can occur through signaling pathways involving p38 MAPK and Akt protein kinases.
These data indicate that downregulation of HMW TMs occurs basically in SCCE and the activation of MEK/ERK and PI3K/Akt pathways as well as the epigenetic mechanism of promoter hypermethylation play important role in TM1 suppression in SCCE.