Please use this identifier to cite or link to this item:
|Title:||Functional roles of SRC signaling in pancreatic cancer: Recent insights provide novel therapeutic opportunities.||Austin Authors:||Poh, Ashleigh R;Ernst, Matthias||Affiliation:||Olivia Newton-John Cancer Research Institute
La Trobe University School of Cancer Medicine, Melbourne, VIC, 3084, Australia.
|Issue Date:||Jun-2023||Date:||2023||Publication information:||Oncogene 2023; 42(22)||Abstract:||Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignant disease with a 5-year survival rate of <10%. Aberrant activation or elevated expression of the tyrosine kinase c-SRC (SRC) is frequently observed in PDAC and is associated with a poor prognosis. Preclinical studies have revealed a multifaceted role for SRC activation in PDAC, including promoting chronic inflammation, tumor cell proliferation and survival, cancer cell stemness, desmoplasia, hypoxia, angiogenesis, invasion, metastasis, and drug resistance. Strategies to inhibit SRC signaling include suppressing its catalytic activity, inhibiting protein stability, or by interfering with signaling components of the SRC signaling pathway including suppressing protein interactions of SRC. In this review, we discuss the molecular and immunological mechanisms by which aberrant SRC activity promotes PDAC tumorigenesis. We also provide a comprehensive update of SRC inhibitors in the clinic, and discuss the clinical challenges associated with targeting SRC in pancreatic cancer.||URI:||https://ahro.austin.org.au/austinjspui/handle/1/32800||DOI:||10.1038/s41388-023-02701-x||ORCID:||0000-0001-8375-4753
|Journal:||Oncogene||PubMed URL:||37120696||ISSN:||1476-5594||Type:||Journal Article|
|Appears in Collections:||Journal articles|
Show full item record
checked on Dec 7, 2023
Items in AHRO are protected by copyright, with all rights reserved, unless otherwise indicated.