PRSS1 mutation: a possible pathomechanism of pancreatic carcinogenesis and pancreatic cancer.

ABSTRACT:

Background

Previous studies revealed somatic mutations of the cationic trypsinogen gene (PRSS1) in patients with chronic pancreatitis and pancreatic cancer. However, whether PRSS1 mutations trigger pancreatic cancer and/or promote malignant proliferation and metastasis in pancreatic cancer remains largely unclear, as well as the potential underlying mechanisms.

Methods

In the present study, whole-exome sequencing was applied for screening, and the R116C mutation was validated by Sanger sequencing. Phosphorylation antibody array, RNA-Seq, and RT-qPCR were adopted to screen and validate that R116C mutation promoted pancreatic cancer progression via the JAK1-STAT5 pathway.

Results

It showed that migration and invasion were significantly increased in R116C-bearing PANC-1

SUBMITTER: Liu Q 

PROVIDER: S-EPMC6744682 | biostudies-literature | 2019 Sep

REPOSITORIES: biostudies-literature