4 results on '"Corano Scheri, Katia"'
Search Results
2. HGF/c-Met pathway in seminoma and non-seminoma cell lines: role in cell invasion
- Author
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CORANO SCHERI, Katia, Leonetti, Erica, Gesualdi, L., Ricci, G., and Catizone, Angiolina
- Subjects
TGCTs ,HGF ,c-MET, HGF, TGCTs ,c-MET - Published
- 2016
3. c-Src Recruitment is Involved in c-MET-Mediated Malignant Behaviour of NT2D1 Non-Seminoma Cells.
- Author
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Leonetti, Erica, Gesualdi, Luisa, Corano Scheri, Katia, Dinicola, Simona, Fattore, Luigi, Masiello, Maria Grazia, Cucina, Alessandra, Mancini, Rita, Bizzarri, Mariano, Ricci, Giulia, and Catizone, Angela
- Subjects
CANCER treatment ,GERM cell tumors ,CANCER chemotherapy ,DRUG resistance ,HEPATOCYTE growth factor ,SEMINOMA - Abstract
c-MET pathway over-activation is the signature of malignancy acquisition or chemotherapy resistance of many cancers. We recently demonstrated that type II Testicular Germ Cell Tumours (TGCTs) express c-MET receptor. In particular, we elucidated that the non-seminoma lesions express c-MET protein at higher level, compared with the seminoma ones. In line with this observation, NTERA-2 clone D1 (NT2D1) non-seminoma cells increase their proliferation, migration and invasion in response to Hepatocyte Growth Factor (HGF). One of the well-known adaptor-proteins belonging to c-MET signaling cascade is c-Src. Activation of c-Src is related to the increase of aggressiveness of many cancers. For this reason, we focused on the role of c-Src in c-MET-triggered and HGF-dependent NT2D1 cell activities. In the present paper, we have elucidated that this adaptor-protein is involved in HGF-dependent NT2D1 cell proliferation, migration and invasion, since Src inhibitor-1 administration abrogates these responses. Despite these biological evidences western blot analyses have not revealed the increase of c-Src activation because of HGF administration. However, notably, immunofluorescence analyses revealed that cytoplasmic and membrane-associated localization of c-Src shifted to the nuclear compartment after HGF stimulation. These results shed new light in the modality of HGF-dependent c-Src recruitment, and put the basis for novel investigations on the relationship between c-Src, and TGCT aggressiveness. [ABSTRACT FROM AUTHOR]
- Published
- 2019
- Full Text
- View/download PDF
4. c-MET receptor as potential biomarker and target molecule for malignant testicular germ cell tumors
- Author
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Corano Scheri, K, Leonetti, E, Laino, L, Gigantino, V, Gesualdi, L, Grammatico, P, Bizzari, M, Franco, R, Oosterhuis, Jw, Stoop, H, Looijenga, Lhj, Ricci, G, Catizone, A., Corano Scheri, Katia, Leonetti, Erica, Laino, Luigi, Gigantino, Vincenzo, Gesualdi, Luisa, Grammatico, Paola, Bizzari, Mariano, Franco, Renato, Wolter Oosterhuis, J, Stoop, Han, Looijenga, Leendert, Ricci, Giulia, Catizone., Angela, and Pathology
- Subjects
c-MET inhibitors ,0301 basic medicine ,endocrine system ,Cancer therapy ,TGCTs ,C-MET inhibitor ,HGF ,c-MET ,cancer therapy ,03 medical and health sciences ,030104 developmental biology ,0302 clinical medicine ,Oncology ,TGCT ,030220 oncology & carcinogenesis ,C-MET - Abstract
Type II testicular germ cell tumors (TGCTs) represent the most frequent malignancy in Caucasian males (20-40 years). Even if diagnosed with disseminated disease, > 80% of patients are cured; however, a small percentage of cases progress and result in death. It is commonly accepted that these cancers arise from a disturbed testicular embryonic niche that leads to the block of gonocyte differentiation. The subsequent development of the invasive seminomas and nonseminomas is due to a combination of genetic, epigenetic and microenvironmentbased alterations (genvironment). Hepatocyte growth factor (HGF) is present in the testicular microenvironment, together with its receptor c-MET, from early embryonic development to an adult stage. In addition, c-MET is a well-known proto-oncogene involved in the onset and progression of various human cancers. Herein, we have investigated the expression and availability of HGF and c-MET in TCam-2, NCCIT and NT2D1 cells, which are type II (T)GCT representative cell lines, and the effect of c-MET activation/repression on the regulation of cancerous biological processes. We found that NT2D1 cells increase their proliferation, polarized migration, and invasion in response to HGF administration. NCCIT cells respond to HGF stimulation only partially, whereas TCam-2 cells do not respond to HGF, at least according to the investigated parameters. Interestingly, the immunohistochemical study of c-MET distribution in TGCTs confirm its presence in both seminoma and non-seminoma lesions with different patterns. Notably, we found the highest c-MET immunoreactivity in the epithelial elements of the various components of TGCTs: teratoma, yolk sac tumor and choriocarcinoma. Type II testicular germ cell tumors (TGCTs) represent the most frequent malignancy in Caucasian males (20-40 years). Even if diagnosed with disseminated disease, > 80% of patients are cured; however, a small percentage of cases progress and result in death. It is commonly accepted that these cancers arise from a disturbed testicular embryonic niche that leads to the block of gonocyte differentiation. The subsequent development of the invasive seminomas and nonseminomas is due to a combination of genetic, epigenetic and microenvironmentbased alterations (genvironment). Hepatocyte growth factor (HGF) is present in the testicular microenvironment, together with its receptor c-MET, from early embryonic development to an adult stage. In addition, c-MET is a well-known proto-oncogene involved in the onset and progression of various human cancers. Herein, we have investigated the expression and availability of HGF and c-MET in TCam-2, NCCIT and NT2D1 cells, which are type II (T)GCT representative cell lines, and the effect of c-MET activation/repression on the regulation of cancerous biological processes. We found that NT2D1 cells increase their proliferation, polarized migration, and invasion in response to HGF administration. NCCIT cells respond to HGF stimulation only partially, whereas TCam-2 cells do not respond to HGF, at least according to the investigated parameters. Interestingly, the immunohistochemical study of c-MET distribution in TGCTs confirm its presence in both seminoma and non-seminoma lesions with different patterns. Notably, we found the highest c-MET immunoreactivity in the epithelial elements of the various components of TGCTs: teratoma, yolk sac tumor and choriocarcinoma.
- Published
- 2018
- Full Text
- View/download PDF
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