SU11274 suppresses proliferation and motility of pancreatic cancer cells

Tomizawa, M.; Shinozaki, Fuminobu; Motoyoshi, Yasufumi; Sugiyama, Takao; Yamamoto, Shozo; Ishige, Naoki

doi:10.3892/ol.2015.3452

Cited by 2 publications

(1 citation statement)

References 21 publications

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“…recently reported that c-MET inhibitors with multikinase activity like crizotinib may exhibit less activity in ovarian cancer than c-MET specific drugs34. SU11274 is a selective inhibitor of c-MET, which has been shown to suppress the proliferation of hepatocellular carcinoma cells and pancreatic cancer cells3536. Firtina Karagonlar et al .…”

Section: Discussionmentioning

confidence: 99%

c-MET as a Potential Therapeutic Target in Ovarian Clear Cell Carcinoma

Kim

Yoon

Ryu

et al. 2016

Sci Rep

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In this study, we investigated the therapeutic effects of c-MET inhibition in ovarian clear cell carcinoma (OCCC). Expression levels of c-MET in the epithelial ovarian cancers (EOCs) and normal ovarian tissues were evaluated using real-time PCR. To test the effects of c-MET inhibitors in OCCC cell lines, we performed MTT and apoptosis assays. We used Western blots to evaluate the expression of c-MET and its down-stream pathway. In vivo experiments were performed to test the effects of c-MET inhibitor on tumor growth in orthotopic mouse xenografts of OCCC cell line RMG1 and a patient-derived tumor xenograft (PDX) model of OCCC. c-MET expression was significantly greater in OCCCs compared with serous carcinomas and normal ovarian tissues (p < 0.001). In in vitro study, inhibition of c-MET using c-MET inhibitors (SU11274 or crizotinib) significantly decreased the proliferation, and increased the apoptosis of OCCC cells. SU11274 decreased expression of the p-c-MET proteins and blocked the phosphorylation of down-stream proteins Akt and Erk. Furthermore, SU11274 treatment significantly decreased the in vivo tumor weight in xenograft models of RMG1 cell and a PDX model for OCCC compared to control (p = 0.004 and p = 0.009, respectively).

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Section: Discussionmentioning

confidence: 99%

c-MET as a Potential Therapeutic Target in Ovarian Clear Cell Carcinoma

Kim

Yoon

Ryu

et al. 2016

Sci Rep

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Targeting the C-MET/HGF Signaling Pathway in Pancreatic Ductal Adenocarcinoma

Ghanaatgar-Kasbi

Khorrami

Avan

et al. 2019

CPD

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The c-mesenchymal-epithelial transition factor (c-MET) is involved in the tumorigenesis of various cancers. HGF/Met inhibitors are now attracting considerable interest due to their anti-tumor activity in multiple malignancies such as pancreatic cancer. It is likely that within the next few years, HGF/Met inhibitors will become a crucial component for cancer management. In this review, we summarize the role of HGF/Met pathway in the pathogenesis of pancreatic cancer, with particular emphasize on HGF/Met inhibitors in the clinical setting, including Cabozantinib (XL184, BMS-907351), Crizotinib (PF-02341066), MK-2461, Merestinib (LY2801653), Tivantinib (ARQ197), SU11274, Onartuzumab (MetMab), Emibetuzumab (LY2875358), Ficlatuzumab (AV- 299), Rilotumumab (AMG 102), and NK4 in pancreatic cancer.

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SU11274 suppresses proliferation and motility of pancreatic cancer cells

Cited by 2 publications

References 21 publications

c-MET as a Potential Therapeutic Target in Ovarian Clear Cell Carcinoma

c-MET as a Potential Therapeutic Target in Ovarian Clear Cell Carcinoma

Targeting the C-MET/HGF Signaling Pathway in Pancreatic Ductal Adenocarcinoma

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