Musashi2 promotes EGF-induced EMT in pancreatic cancer via ZEB1-ERK/MAPK signaling.

ABSTRACT:

Background

Our previous study showed Musashi2 (MSI2) promoted chemotherapy resistance and pernicious biology of pancreatic cancer (PC) by down-regulating Numb and p53. We further explored the novel molecular mechanism involving its oncogenic role in PC development.

Methods

We investigated the potential role and mechanism of MSI2 in EGF-induced EMT in PC in vitro and vivo.

Results

EGF enhanced EGFR (epidermal growth factor receptor) phosphorylation, induced EMT and activated ZEB1-ERK/MAPK signaling in 2 PC cells. However, MSI2 silencing reversed EGF stimulated function, including inhibiting EGF-promoted EMT-like cell morphology and EGF-enhanced cell invasion and migration. Meanwhile, MSI2 silencing inhibited EGF-enhanced EGFR phosphorylation at tyrosine 1068 and revers

SUBMITTER: Sheng W 

PROVIDER: S-EPMC6967093 | biostudies-literature | 2020 Jan

REPOSITORIES: biostudies-literature