Questions and Answers (3) View all
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Answer added in Cell Cycle12 M phase cell cycle arrestIf you stain DNA only , you should see if cells exhibit an interphasic nucleus or if chromosomes are condensing. You can also simply stain your cells ... [more]
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Answer added in Cell Biology3 Fibroblast growth curvesPlease be careful that at the end of the kinetics the cells just reach confluency. otherwise you will have an early plateau. Typically, we seed 25 00... [more]
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Answer added in Cell Biology7 Multi-nucleation of MCF-7 cellBinucleate cells can result from a failure in late mitosis or cytokinesis. If those cells try and fail to divide again, you will see multinucleate cel... [more]
Publications (34) View all
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Article: Cyclin A2 and c-myc mRNA expression in ethinyl estradiol induced liver proliferation.
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ABSTRACT: The time-course of c-myc and cyclin A2 mRNA expression was determined in the liver of male Sprague-Dawley rats during transient liver cell proliferation induced by a single dose of ethinyl estradiol (EE), and was compared to that during liver regeneration following two-thirds hepatectomy (PH). Cell proliferation was assessed in terms of 5'-bromodeoxyuridine (BrdU) labeling. EE administration and PH both increased BrdU labeling between 18 and 48 h, with peak values at 18 and 24 h. An early (2 h) increase in BrdU labeling was observed after EE but not PH. Maximal increases in cyclin A2 mRNA levels and BrdU labeling coincided after both EE and PH, and cyclin A2 mRNA expression was proportional to the intensity of the proliferative response. In contrast, the degree of c-myc mRNA expression was similar after EE administration and PH, but the time course was different: c-myc gene expression rose concomitantly with DNA replication after EE, while after PH it increased during the prereplicative phase. This indicates that the pattern of c-myc gene expression in the liver is strongly related to the type of proliferative response.Molecular and Cellular Endocrinology 09/1998; 143(1-2):107-16. · 4.19 Impact Factor -
Article: Cyclin A: function and expression during cell proliferation.
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ABSTRACT: Cyclin A is a key regulatory protein which, in mammalian cells, is involved in both S phase and the G2/M transition of the cell cycle through its association with distinct cdks. Several lines of evidence have also implicated cyclin A in carcinogenesis. Our review concentrates on the role of cyclin A in S phase, in the S/G2 transition and in human carcinogenesis; it will also discuss the transcriptional regulation of cyclin A gene.Progress in cell cycle research 01/1995; 1:115-23. -
Article: KIF20A mRNA and its product MKlp2 are increased during hepatocyte proliferation and hepatocarcinogenesis.
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ABSTRACT: Mitotic kinesin-like protein 2 (MKlp2), a microtubule-associated motor, is required during mitosis exit for the final step of cytokinesis. It also contributes to retrograde vesicular trafficking from the Golgi apparatus to the endoplasmic reticulum in interphase. The KIF20A gene encoding MKlp2 is controlled by the E2F-retinoblastoma protein-p16 pathway, and its widely expressed mRNA is found in fetal and proliferating adult tissues. The expression pattern and function of MKlp2 in the adult liver, however, have not been investigated. We report herein that MKlp2 transiently accumulates in vivo during mouse liver regeneration after partial hepatectomy and is strongly overexpressed in preneoplastic and neoplastic mouse liver. In vitro in mitogen-stimulated primary hepatocytes, MKlp2 accumulated in the nucleus during the G2 phase of the cell cycle coincident with the mitotic kinase Aurora B. Human hepatoma cell lines exhibited high levels of MKlp2; however, it was undetectable in normal human hepatocytes. RNAi-mediated MKlp2 knockdown in hepatoma cells induced polyploidization consistent with its essential function in promoting cytokinesis and inhibited cell proliferation without inducing apoptosis. KIF20A mRNA was strongly accumulated in a large series of human hepatocellular carcinomas, with the highest expression observed in tumors with genomic instability. Accumulation of MKlp2 in normal proliferating, preneoplastic, and transformed hepatocytes suggests that MKlp2 contributes to both normal and pathologic hepatocyte proliferation and is linked to tumor aggressiveness in human hepatocellular carcinomas.American Journal Of Pathology 11/2011; 180(1):131-40. · 4.89 Impact Factor -
Article: Priming and potentiation of DNA damage response by fibronectin in human colon cancer cells and tumor-derived myofibroblasts.
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ABSTRACT: We have previously shown that the genotoxin-induced apoptosis in mouse embryo fibroblasts was enhanced by the extracellular matrix protein fibronectin (FN). In the present study, we tested the hypothesis that FN regulates the DNA damage response (DDR) signaling pathways in HCT116 (p53-wt) and HT29 (p53-mut) human colon cancer cells and tumor-derived myofibroblasts. DNA damage recognition mechanisms were analyzed by immunofluorescence staining, cell cycle analysis and immunoblotting addressed at specific molecular sensors and executors involved in the DDR pathways. The results show that FN, but not collagen type IV or Matrigel, initiates and potentiates the DDR to the anticancer drug cisplatin in an α5 integrin and cell cycle-dependent manner (S and G2/M phases) in human colon cancer cells. Accordingly, we demonstrate that adhesion of HCT116 cells to FN upregulated the expression of α5 integrin FN receptors at the cell surface. These FN-induced DDR pathways include the concerted phosphorylation of histone H2AX on Ser139 detected as nuclear foci (γ-H2AX, 15 and 25 kDa forms), of ataxia telangiectasia mutated (ATM-Ser1981), checkpoint kinase 2 (CHK2-Thr68, 62 and 67 kDa) and p53-Ser15. These FN-induced γ-H2AX signals were interrupted or attenuated by selective inhibitors acting on the DDR pathway kinases, including wortmannin (targeting the phosphatidylinositol-3-kinase-related protein kinases, PIKK), KU55933 (ATM), NU7026 (DNA-dependent protein kinase catalytic subunit, DNA-PK-cs) and SP600125 (JNK2, stress activated protein kinase/c-Jun N-terminal kinase-2). Adhesion to FN also potentiated the γ-H2AX signals and the cytotoxic effects of cisplatin in human colon tumor-derived myofibroblasts. These data provide evidence that FN promotes DNA damage recognition and chemosensitization to cisplatin via the potentiation of the DNA damage signaling responses in human colon cancer cells and tumor-derived myofibroblasts.International Journal of Oncology 08/2011; 39(2):393-400. · 2.40 Impact Factor -
Article: Comparison of biochemical properties of DNA-topoisomerase I from normal and regenerating liver.
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ABSTRACT: Biochemical properties of topoisomerase I from normal and regenerating rat liver were analysed using crude or fractionated nuclear extracts. We could not detect significative change in topoisomerase I content or activity (magnesium stimulation and inhibition by ATP) during the course of liver regeneration. Topoisomerase I can be resolved into two species of 97 kDa and 100 kDa, with the same pI of 8.2-8.6 as shown by two dimensional gel electrophoresis. The two polypeptides contained a non-phosphorylated precursor and others forms with variable degrees of phosphorylation. In-vitro dephosphorylation with alkaline phosphatase leads to the disappearance of the phosphorylated forms and inactivation of the enzyme. The affinity of topoisomerase I for chromatin (measured by salt elution) differs markedly between normal and regenerating liver: nearly 50% of topoisomerase I remained bound to the chromatin from normal liver at 250 mM NaCl whereas it was completely eluted from 24-h-regenerating-liver nuclei. The biological significance of these results is discussed.European Journal of Biochemistry 12/1992; 210(1):359-64. · 3.58 Impact Factor
