| Title: |
Targeting hgf/c-met axis in pancreatic cancer |
| Authors: |
Pothula, SP; Xu, Z; Goldstein, D; Pirola, RC; Wilson, JS; Apte, MV |
| Source: |
urn:ISSN:1661-6596 ; urn:ISSN:1422-0067 ; International Journal of Molecular Sciences, 21, 23, 1-18 |
| Publisher Information: |
MDPI |
| Publication Year: |
2020 |
| Collection: |
UNSW Sydney (The University of New South Wales): UNSWorks |
| Subject Terms: |
3101 Biochemistry and Cell Biology; 31 Biological Sciences; 3404 Medicinal and Biomolecular Chemistry; 34 Chemical Sciences; 3107 Microbiology; Pancreatic Cancer; Digestive Diseases; Rare Diseases; Orphan Drug; Cancer; 2.1 Biological and endogenous factors; Animals; Biomarkers; Tumor; Gene Expression Regulation; Neoplastic; Hepatocyte Growth Factor; Humans; Neoplasm Staging; Neovascularization; Pathologic; Pancreatic Neoplasms; Proto-Oncogene Proteins c-met; Signal Transduction; Tumor Microenvironment; HGF-c-MET; Stromal-tumour interactions; anzsrc-for: 3101 Biochemistry and Cell Biology; anzsrc-for: 31 Biological Sciences; anzsrc-for: 3404 Medicinal and Biomolecular Chemistry |
| Description: |
Pancreatic cancer (pancreatic ductal adenocarcinoma (PDAC/PC)) has been an aggressive disease that is associated with early metastases. It is characterized by dense and collagenous desmoplasia/stroma, predominantly produced by pancreatic stellate cells (PSCs). PSCs interact with cancer cells as well as other stromal cells, facilitating disease progression. A candidate growth factor pathway that may mediate this interaction is the hepatocyte growth factor (HGF)/c-MET pathway. HGF is produced by PSCs and its receptor c-MET is expressed on pancreatic cancer cells and endothelial cells. The current review discusses the role of the MET/HGF axis in tumour progression and dissemination of pancreatic cancer. Therapeutic approaches that were developed targeting either the ligand (HGF) or the receptor (c-MET) have not been shown to translate well into clinical settings. We discuss a two-pronged approach of targeting both the components of this pathway to interrupt the stromal–tumour interactions, which may represent a potential therapeutic strategy to improve outcomes in PC. |
| Document Type: |
article in journal/newspaper |
| File Description: |
application/pdf |
| Language: |
unknown |
| Relation: |
https://hdl.handle.net/1959.4/unsworks_73863; https://doi.org/10.3390/ijms21239170 |
| DOI: |
10.3390/ijms21239170 |
| Availability: |
https://hdl.handle.net/1959.4/unsworks_73863; https://unsworks.unsw.edu.au/bitstreams/a8dfb185-1b23-47f5-ba41-2532ce069229/download; https://doi.org/10.3390/ijms21239170 |
| Rights: |
open access ; https://purl.org/coar/access_right/c_abf2 ; CC BY ; https://creativecommons.org/licenses/by/4.0/ ; free_to_read |
| Accession Number: |
edsbas.A75DBB66 |
| Database: |
BASE |