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3 results on '"Nicoloso MS"'

1. E2F1-regulated microRNAs impair TGFbeta-dependent cell-cycle arrest and apoptosis in gastric cancer.

Author

Petrocca F, Visone R, Onelli MR, Shah MH, Nicoloso MS, de Martino I, Iliopoulos D, Pilozzi E, Liu CG, Negrini M, Cavazzini L, Volinia S, Alder H, Ruco LP, Baldassarre G, Croce CM, and Vecchione A

Subjects
Adenocarcinoma metabolism, Adenocarcinoma pathology, Apoptosis Regulatory Proteins genetics, Apoptosis Regulatory Proteins metabolism, Bcl-2-Like Protein 11, Cell Cycle Proteins genetics, Cell Cycle Proteins metabolism, Cell Line, Tumor, Cell Proliferation, Cyclin-Dependent Kinase Inhibitor p21 genetics, Cyclin-Dependent Kinase Inhibitor p21 metabolism, DNA-Binding Proteins genetics, DNA-Binding Proteins metabolism, E2F1 Transcription Factor genetics, Feedback, Physiological, Humans, Membrane Proteins genetics, Membrane Proteins metabolism, Minichromosome Maintenance Complex Component 7, Nuclear Proteins genetics, Nuclear Proteins metabolism, Proto-Oncogene Proteins genetics, Proto-Oncogene Proteins metabolism, RNA, Messenger metabolism, Stomach Neoplasms metabolism, Stomach Neoplasms pathology, Time Factors, Transfection, Up-Regulation, Adenocarcinoma genetics, Apoptosis genetics, Cell Cycle genetics, E2F1 Transcription Factor metabolism, Gene Expression Regulation, Neoplastic, MicroRNAs metabolism, RNA Processing, Post-Transcriptional, Stomach Neoplasms genetics, Transforming Growth Factor beta metabolism
Abstract

Deregulation of E2F1 activity and resistance to TGFbeta are hallmarks of gastric cancer. MicroRNAs (miRNAs) are small noncoding RNAs frequently misregulated in human malignancies. Here we provide evidence that the miR-106b-25 cluster, upregulated in a subset of human gastric tumors, is activated by E2F1 in parallel with its host gene, Mcm7. In turn, miR-106b and miR-93 regulate E2F1 expression, establishing a miRNA-directed negative feedback loop. Furthermore, upregulation of these miRNAs impairs the TGFbeta tumor suppressor pathway, interfering with the expression of CDKN1A (p21(Waf1/Cip1)) and BCL2L11 (Bim). Together, these results suggest that the miR-106b-25 cluster is involved in E2F1 posttranscriptional regulation and may play a key role in the development of TGFbeta resistance in gastric cancer.

Published
2008
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2. Fez1/Lzts1 absence impairs Cdk1/Cdc25C interaction during mitosis and predisposes mice to cancer development.

Author

Vecchione A, Baldassarre G, Ishii H, Nicoloso MS, Belletti B, Petrocca F, Zanesi N, Fong LY, Battista S, Guarnieri D, Baffa R, Alder H, Farber JL, Donovan PJ, and Croce CM

Subjects
Animals, Antineoplastic Agents pharmacology, Carcinogens, Cell Division, Cells, Cultured, Chromosome Segregation, Dimethylnitrosamine analogs & derivatives, Fibroblasts metabolism, Fibroblasts pathology, Mice, Mice, Knockout, Molecular Sequence Data, Nocodazole pharmacology, Paclitaxel pharmacology, Stomach Neoplasms chemically induced, Stomach Neoplasms genetics, Tumor Suppressor Proteins genetics, CDC2 Protein Kinase physiology, Cell Cycle Proteins physiology, Cell Transformation, Neoplastic, Mitosis, Stomach Neoplasms pathology, Tumor Suppressor Proteins physiology, cdc25 Phosphatases physiology
Abstract

The FEZ1/LZTS1 (LZTS1) protein is frequently downregulated in human cancers of different histotypes. LZTS1 is expressed in normal tissues, and its introduction in cancer cells inhibits cell growth and suppresses tumorigenicity, owing to an accumulation of cells in G2/M. Here, we define its role in cell cycle regulation and tumor progression by generating Lzts1 knockout mice. In Lzts1(-/-) mouse embryo fibroblasts (MEFs), Cdc25C degradation was increased during M phase, resulting in decreased Cdk1 activity. As a consequence, Lzts1(-/-) MEFs showed accelerated mitotic progression, resistance to taxol- and nocodazole-induced M phase arrest, and improper chromosome segregation. Accordingly, Lzts1 deficiency was associated with an increased incidence of both spontaneous and carcinogen-induced cancers in mice.

Published
2007
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3. p27(Kip1)-stathmin interaction influences sarcoma cell migration and invasion.

Author

Baldassarre G, Belletti B, Nicoloso MS, Schiappacassi M, Vecchione A, Spessotto P, Morrione A, Canzonieri V, and Colombatti A

Subjects
Animals, Cell Adhesion, Cell Cycle Proteins genetics, Cell Line, Tumor, Cells, Cultured, Cyclin-Dependent Kinase Inhibitor p27, Enzyme Inhibitors metabolism, Extracellular Matrix metabolism, Fibroblasts cytology, Fibroblasts physiology, Fibronectins metabolism, Genes, Tumor Suppressor, Humans, Mice, Mice, Inbred C57BL, Mice, Knockout, Microtubule Proteins genetics, Microtubules metabolism, Neoplasm Metastasis, Phenotype, Phosphoproteins genetics, Stathmin, Tubulin genetics, Tubulin metabolism, Tumor Suppressor Proteins genetics, Cell Cycle Proteins metabolism, Cell Movement, Microtubule Proteins metabolism, Phosphoproteins metabolism, Sarcoma metabolism, Sarcoma pathology, Tumor Suppressor Proteins metabolism
Abstract

Emerging evidences suggest that cyclin-dependent kinase inhibitors (CKIs) can regulate cellular functions other than cell cycle progression, such as differentiation and migration. Here, we report that cytoplasmic expression of p27(kip1) affects microtubule (MT) stability following cell adhesion on extracellular matrix (ECM) constituents. This p27(kip1) activity is due to its ability to bind and impair the function of the MT-destabilizing protein stathmin. Accordingly, upregulation of p27(kip1) or downregulation of stathmin expression results in the inhibition of mesenchymal cell motility. Moreover, high stathmin and low cytoplasmic p27(kip1) expression correlate with the metastatic phenotype of human sarcomas in vivo. This study provides a functional link between proliferation and invasion of tumor cells based on diverse activities of p27(kip1) in different subcellular compartments.

Published
2005
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