Characterization of HGF/Met Signaling in Cell Lines Derived From Urothelial Carcinoma of the Bladder
| العنوان: | Characterization of HGF/Met Signaling in Cell Lines Derived From Urothelial Carcinoma of the Bladder |
|---|---|
| المؤلفون: | Young H. Lee, Piyush K. Agarwal, Donald P. Bottaro, Andrea B. Apolo |
| المصدر: | Cancers, Vol 6, Iss 4, Pp 2313-2329 (2014) Cancers Volume 6 Issue 4 Pages 2313-2329 |
| بيانات النشر: | MDPI AG, 2014. |
| سنة النشر: | 2014 |
| مصطلحات موضوعية: | Cancer Research, Pathology, medicine.medical_specialty, Cabozantinib, lcsh:RC254-282, Article, chemistry.chemical_compound, Paracrine signalling, tumor cell invasion, medicine, urothelial carcinoma, Bladder cancer, Crizotinib, Cell growth, business.industry, medicine.disease, lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens, hepatocyte growth factor, tumor growth, Oncology, chemistry, Cell culture, Cancer research, Met, bladder cancer, Hepatocyte growth factor, Signal transduction, business, medicine.drug |
| الوصف: | There is mounting evidence of oncogenic hepatocyte growth factor (HGF)/Met signaling in urothelial carcinoma (UC) of the bladder. The effects of three kinase inhibitors, cabozantinib, crizotinib and EMD1214063, on HGF-driven signaling and cell growth, invasion and tumorigenicity were analyzed in cultured UC cell lines. SW780 xenograft growth in SCID and human HGF knock-in SCID (hHGF/SCID) mice treated with cabozantinib or vehicle, as well as tumor levels of Met and pMet, were also determined. Met content was robust in most UC-derived cell lines. Basal pMet content and effector activation state in quiescent cells were low, but significantly enhanced by added HGF, as were cell invasion, proliferation and anchorage independent growth. These HGF-driven effects were reversed by Met inhibitor treatment. Tumor xenograft growth was significantly higher in hHGF/SCID mice vs. SCID mice and significantly inhibited by cabozantinib, as was tumor phospho-Met content. These studies indicate the prevalence and functionality of the HGF/Met signaling pathway in UC cells, suggest that paracrine HGF may contribute to UC tumor growth and progression, and that support further preclinical investigation of Met inhibitors for the treatment of UC is warranted. |
| وصف الملف: | application/pdf |
| اللغة: | English |
| تدمد: | 2072-6694 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::55fd953e7aaebbe340202ee0ab74c889Test http://www.mdpi.com/2072-6694/6/4/2313Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....55fd953e7aaebbe340202ee0ab74c889 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 20726694 |
|---|