Published online May 28, 2021. doi: 10.3748/wjg.v27.i20.2507
Peer-review started: December 31, 2020
First decision: February 23, 2021
Revised: March 4, 2021
Accepted: April 9, 2021
Article in press: April 9, 2021
Published online: May 28, 2021
The receptor protein tyrosine kinase RON belongs to the c-MET proto-oncogene family. Research has shown that RON has a role in cancer pathogenesis, which places RON on the frontline of the development of novel cancer therapeutic strategies. Hepatobiliary and pancreatic (HBP) cancers have a poor prognosis, being reported as having higher rates of cancer-related death. Therefore, to combat these malignant diseases, the mechanism underlying the aberrant expression and signaling of RON in HBP cancer pathogenesis, and the development of RON as a drug target for therapeutic intervention should be investigated. Abnormal RON expression and signaling have been identified in HBP cancers, and also act as tumorigenic determinants for HBP cancer malignant behaviors. In addition, RON is emerging as an important mediator of the clinical prognosis of HBP cancers. Thus, not only is RON significant in HBP cancers, but also RON-targeted therapeutics could be developed to treat these cancers, for example, therapeutic monoclonal antibodies and small-molecule inhibitors. Among them, antibody-drug conjugates have become increasingly popular in current research and their potential as novel anti-cancer biotherapeutics will be determined in future clinical trials.
Core Tip: The role of RON in cancer pathogenesis has received increasing research attention. Hepatobiliary and pancreatic (HBP) cancers have a poor prognosis, being reported as having higher rates of cancer-related death because of their high rates of recurrence, metastasis, and invasiveness, and their lack of sensitivity to chemotherapy. In this review, we discuss how RON functions in HBP cancer pathogenesis, as well as its potential role as a therapeutic target in HBP cancers.