المؤلفون: Pier Paolo Scaglioni, Andrea Rabellino, Cristina Andreani

المصدر: Current Issues in Molecular Biology
Volume 35
Issue 1
Pages 109-126

مصطلحات موضوعية: 0301 basic medicine, Angiogenesis, SUMO protein, Neovascularization, Physiologic, Biology, Neovascularization, 03 medical and health sciences, Roles, 0302 clinical medicine, Ubiquitin, medicine, Animals, Humans, Phosphorylation, Receptor, Neovascularization, Pathologic, Receptors, Notch, Mechanism (biology), Ubiquitination, Endothelial Cells, General Medicine, SUMOylation, Cell biology, 030104 developmental biology, Receptors, Vascular Endothelial Growth Factor, 030220 oncology & carcinogenesis, Protein processing, biology.protein, medicine.symptom, Protein Processing, Post-Translational, Signal Transduction, Regulation

الوصف: The generation of new blood vessels from the existing vasculature is a dynamic and complex mechanism known as angiogenesis. Angiogenesis occurs during the entire lifespan of vertebrates and participates in many physiological processes. Furthermore, angiogenesis is also actively involved in many human diseases and disorders, including cancer, obesity and infections. Several inter-connected molecular pathways regulate angiogenesis, and post-translational modifications, such as phosphorylation, ubiquitination and SUMOylation, tightly regulate these mechanisms and play a key role in the control of the process. Here, we describe in detail the roles of ubiquitination and SUMOylation in the regulation of angiogenesis.

وصف الملف: application/pdf

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::32a8bb3309ac8d072dfd9aa7097da233Test

المؤلفون: Barbara Belletti, Maria Elexpuru Zabaleta, Augusto Amici, Valentina Gambini, Cristina Kalogris, Manuela Iezzi, Cristiano Lucci, Cristina Andreani, Chiara Garulli, Stefania Pucciarelli, Cristina Marchini, Lucia Pietrella, Caterina Bartolacci, Mara Giangrossi, Martina Tilio

المصدر: Biochemical Pharmacology. 90:226-234

مصطلحات موضوعية: Programmed cell death, Cell Survival, Apoptosis, Breast Neoplasms, Mice, Inbred Strains, Biochemistry, Mice, Necrosis, Random Allocation, chemistry.chemical_compound, Cyclin D1, Downregulation and upregulation, Cell Movement, Cell Line, Tumor, Dihydrofolate reductase, Animals, Humans, Sanguinarine, Viability assay, STAT3, Neoplasms, Basal Cell, Benzophenanthridines, Pharmacology, biology, Isoquinolines, Antineoplastic Agents, Phytogenic, Molecular biology, Neoplasm Proteins, Tumor Burden, Tetrahydrofolate Dehydrogenase, Methotrexate, chemistry, Drug Resistance, Neoplasm, biology.protein, Cancer research, Folic Acid Antagonists, Female, Neoplasm Transplantation

الوصف: Basal-like breast cancer (BLBC) remains a great challenge because of its clinically aggressive nature and lack of effective targeted therapy. We analyzed the potential anti-neoplastic effects of sanguinarine, a natural benzophenanthridine alkaloid, against BLBC cells. Sanguinarine treatment resulted in a reduction of cell migration, in a dose-dependent inhibition of cell viability and in the induction of cell death by apoptosis in both human (MDA-MB-231 cells) and mouse (A17 cells) in vitro models of BLBC. In vivo experiments demonstrated that oral administration of sanguinarine reduced the development and growth of A17 transplantable tumors in FVB syngeneic mice. Western blotting analysis revealed that suppression of BLBC growth by sanguinarine was correlated with a concurrent upregulation of p27 and downregulation of cyclin D1 and with the inhibition of STAT3 activation. In addition, we identified sanguinarine as a potent inhibitor of dihydrofolate reductase (DHFR), able to impair enzyme activity even in methotrexate resistant MDA-MB-231 cells. These results provide evidence that sanguinarine is a promising anticancer drug for the treatment of BLBC.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::42f416d887041463bd2601213ff54d07Test
https://doi.org/10.1016/j.bcp.2014.05.014Test

المؤلفون: Mauro Provinciali, Barbara Belletti, Maria Elexpuru Zabaleta, Augusto Amici, Cristina Andreani, Manuela Iezzi, Cristina Marchini, Roberta Galeazzi, Fiorenza Orlando, Junbiao Wang, Albana Hysi, Martina Tilio, Chiara Garulli, Lucia Pietrella, Caterina Bartolacci, Valentina Gambini, Cristina Kalogris

مصطلحات موضوعية: 0301 basic medicine, Cancer Research, Time Factors, Receptor, ErbB-2, Pharmacology, Receptor tyrosine kinase, chemistry.chemical_compound, 0302 clinical medicine, Medicine, Protein Isoforms, skin and connective tissue diseases, biology, Penetrance, Metastatic breast cancer, Phenotype, Oncology, 030220 oncology & carcinogenesis, Female, Signal transduction, medicine.drug, Signal Transduction, Cell Survival, Breast Neoplasms, Mice, Transgenic, Lapatinib, 03 medical and health sciences, Inhibitory Concentration 50, Breast cancer, Cell Line, Tumor, Animals, Humans, Genetic Predisposition to Disease, Benzodioxoles, Protein Kinase Inhibitors, Quinazolinones, Dose-Response Relationship, Drug, business.industry, Mammary Neoplasms, Experimental, medicine.disease, Dacomitinib, Alternative Splicing, 030104 developmental biology, chemistry, Drug Resistance, Neoplasm, Cancer research, biology.protein, Quinazolines, business

الوصف: HER2 tyrosine kinase receptor is a validated target in breast cancer therapy. However, increasing evidence points to a major role of Δ16HER2 splice variant commonly coexpressed with HER2 and identified as a clinically important HER2 molecular alteration promoting aggressive metastatic breast cancer. Consistently, mice transgenic for the human Δ16HER2 isoform (Δ16HER2 mice) develop invasive mammary carcinomas with early onset and 100% penetrance. The present study provides preclinical evidence that Δ16HER2 expression confers de novo resistance to standard anti-HER2-therapies such as Lapatinib and acquired resistance to the selective Src inhibitor Saracatinib in breast cancer. Of note, Dacomitinib, an irreversible small molecule pan-HER inhibitor, was able to completely suppress Δ16HER2-driven breast carcinogenesis. Thus, only Dacomitinib may offer benefit in this molecularly defined patient subset by irreversibly inhibiting Δ16HER2 activation.

الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::905e007554f7513a3be0550e5a38e7eeTest
http://hdl.handle.net/11581/394045Test