ArticleOncotarget2014
Crizotinib exhibits antitumor activity by targeting ALK signaling not c-MET in pancreatic cancer.
Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 26 citations in OpenAlex.
- Review
- Identification of Prognostic Markers and Potential Therapeutic Targets using Gene Expression Profiling and Simulation Studies in Pancreatic Cancer.Current computer-aided drug design · 2024Article
- Article
- Treatment optimization of locally advanced and metastatic pancreatic cancer (Review).International journal of oncology · 2021Review
- HGF/c-Met Axis: The Advanced Development in Digestive System Cancer.Frontiers in cell and developmental biology · 2020Review
- Applied precision medicine in metastatic pancreatic ductal adenocarcinoma.Therapeutic advances in medical oncology · 2020Article
- Crizotinib and PARP inhibitors act synergistically by triggering apoptosis in high-grade serous ovarian cancer.Oncotarget · 2019Article
- Promising new treatments for pancreatic cancer in the era of targeted and immune therapies.American journal of cancer research · 2019Review
- HGF/c-MET: A Promising Therapeutic Target in the Digestive System Cancers.International journal of molecular sciences · 2018Review
- [Clinical Advanced in Early-stage ALK-positive Non-small Cell Lung Cancer Patients].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2017Review
- Pancreatic stellate cell: Pandora's box for pancreatic disease biology.World journal of gastroenterology · 2017Review
- Nicotine Reduces Survival via Augmentation of Paracrine HGF-MET Signaling in the Pancreatic Cancer Microenvironment.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016Article
- Novel agents for advanced pancreatic cancer.Oncotarget · 2015Review
- Foretinib inhibits angiogenesis, lymphangiogenesis and tumor growth of pancreatic cancer in vivo by decreasing VEGFR-2/3 and TIE-2 signaling.Oncotarget · 2015Article
- Roles of c-Met and RON kinases in tumor progression and their potential as therapeutic targets.Oncotarget · 2015Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Crizotinib, a c-MET/ALK inhibitor, has exhibited antitumor efficacy in different types of cancers. However, studies regarding Crizotinib in pancreatic cancer have been limited. Thus, we investigated the effect of Crizotinib on pancreatic cancer and its mechanism of action. Crizotinib strongly suppressed the growth and proliferation of pancreatic cancer cells in a dose-dependent manner. Also, it induced apoptosis by modulating its related factors. In the study, with regard to the mechanism of action, Crizotinib did not inhibit c-MET expression on pancreatic cancer cells; instead, it specifically inhibited the activity of ALK, which was identified to be highly expressed on various pancreatic cancer cells and tissues in our study. In 42 different receptor tyrosine kinase (RTKs) array, Crizotinib also strongly inhibited the expression of activated ALK in pancreatic cancer cells, modulating its downstream mediators such as STAT3, AKT, and ERK. Furthermore, Crizotinib inhibited angiogenesis in a mouse Matrigel plug assay as well as the progression of tumor growth in a mouse xenograft model. Taken together, our investigation shows that Crizotinib inhibits the ALK signaling pathway in pancreatic cancer, resulting in cell growth/angiogenesis inhibition and apoptosis induction. We suggest that Crizotinib might be used as a novel therapeutic drug for treating pancreatic cancer.
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