Published online Oct 28, 2019. doi: 10.3748/wjg.v25.i40.6063
Peer-review started: July 16, 2019
First decision: August 18, 2019
Revised: September 3, 2019
Accepted: September 27, 2019
Article in press: September 28, 2019
Published online: October 28, 2019
Processing time: 107 Days and 7.9 Hours
Pancreatic cancer is one of the most common causes of cancer-related deaths worldwide. Current treatment options for patients with pancreatic cancer are very limited, and the clinical outcomes remain unsatisfactory. New therapy targets are necessary to improve the survival rates of pancreatic cancer patients. Insulin-like growth factor 2 mRNA-binding protein 1 (IGF2BP1) plays critical roles in the genesis and development of human cancers. Little is known regarding IGF2BP1 expression and its role in the carcinogenesis or progression of pancreatic ductal adenocarcinoma (PDAC).
Our findings will provide a new therapeutic target for pancreatic cancer.
To study the expression, function, and regulatory mechanisms of IGF2BP1 in pancreatic cancer.
We detected the expression levels of IGF2BP1 and miR-494 in Gene Expression Omnibus datasets and validated in clinical samples by quantitative real-time polymerase chain reaction and Western blot. The relationship between IGF2BP1 expression and clinicopathological factors of pancreatic cancer patients was analyzed. The effect and mechanism of IGF2BP1 on pancreatic cancer cell proliferation were investigated in vitro and in vivo. Analyses were performed to explore underlying mechanisms of IGF2BP1 upregulation in pancreatic cancer and assays were carried out to verify the post- transcriptional regulation of IGF2BP1 by miR-494.
In the present study, we found that IGF2BP1 was upregulated and associated with a poor prognosis of pancreatic cancer patients. We showed that knockdown of IGF2BP1 reduced pancreatic cancer cell proliferation in vitro and in vivo via the AKT signaling pathway. Meanwhile, the frequent upregulation of IGF2BP1 was attributed to the downregulation of miR-494 expression in pancreatic cancer.
IGF2BP1 is upregulated and promotes the proliferation of pancreatic cancer via the AKT signaling pathway. Upregulation of IGF2BP1 is partly due to the silencing of miR-494.
This study provides insight into the role of IGF2BP1 in promoting pancreatic cancer development by activating AKT. IGF2BP1 might be a new therapeutic target for pancreatic cancer.