Juanjuan Tang

Tongji University, Shanghai, Shanghai Shi, China

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Publications (3)11.66 Total impact

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    ABSTRACT: The events leading to Schwannomas development are still largely unknown. Some studies have demonstrated that merlin acts as a tumor suppressor by blocking Ras-mediated signaling. In this study, we analyze the clinical and biological behaviors of seven randomly selected sporadic vestibular Schwannomas removed from the patients. We find that merlin was commonly lost in these Schwannomas, due to loss of merlin expression or phosphorylation status of merlin expression. Heightened CDKs/cyclins signal transduction concomitant with loss of p27 was well correlated with loss of functional merlin in Schwannomas. More, we show that phosphorylated merlin Schwannomas exhibited increased Ras/Rac/PAK signal transduction. That was in agreement with the severe clinical behaviors, i.e., phosphorylation status of merlin increased tumor size in sporadic vestibular Schwannomas. These results led us to suggest that phosphorylated merlin, a kind of type of mutation merlin, is involved in tumorigenesis of sporadic vestibular Schwannomas.
    Molecular and Cellular Biochemistry 02/2009; 324(1-2):201-6. · 2.33 Impact Factor
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    ABSTRACT: NFkappaB/p65 is a transcription factor that can protect or contribute to cell death. Here we show that knockdown of p65 by IkappaBSR or p65 siRNA decreased the cytotoxic effect of DOX on HCT116 (p53+/+) cells, correlating with increased induction of p21. In previous work, we demonstrated that p21 suppressed cell death via its CDK-inhibitory activity. Thus, we propose that the p65 activity is required for p53-dependent cell death through limitation of p53-induced p21 expression. In HCT116 (p53-/-) cells, downregulation of p65 expression enhanced the cytotoxic effect of DOX, due to decreased p21 expression levels. We present evidence that in p53-null tumor cells treated with DOX, p65 was involved in induction of p21 expression by directly binding to the p21 promoter. Our data suggested that both p53 and p65 limited each other's ability to stimulate p21 induction and this mutual repression mechanism was consistent with a model in which both factors were competing for limiting pool of p300/CBP coactivator protein complexes. These findings indicate an association between p21 expression and resistance to cell death through p65, a novel regulatory mechanism in which p21 bridges a transcriptional crosstalk between p53 and p65.
    Biochimica et Biophysica Acta 06/2008; 1783(5):935-40. · 4.66 Impact Factor
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    ABSTRACT: The efficiency of anticancer therapy is often restricted by the development of drug resistance. Here, we report that the doxorubicin (DOX)-resistant MCF-7/Adr cells were more resistant to DOX-treatment than MCF-7 cells. However, an alternative treatment of DOX/TNF-alpha enhanced the cytotoxic effect in multidrug resistant MCF-7/Adr cell line. Treatment of cells with TNF-alpha following doxorubicin (DOX) resulted in a decrease of the activated Rel A/p65 in nuclei. Histone deacetylase 1 (HDAC1) was found to interact with Rel A/p65 in the complex, suggesting that HDAC1 is involved in mediating nuclear export of Rel A/p65. The combined treatment of TNF-alpha/DOX also resulted in a significant decrease of mRNA levels of anti-apoptotic genes, such as the cellular inhibitor of apoptosis-1 (c-IAP1), and the long isoform of B cell leukemia/lymphoma x gene (Bcl-xL), leading to efficient induction of caspase-8 cleavage and cell death. In previous work, we demonstrated that TNF-alpha promotes DOX-induced cell death and anti-cancer effect through downregulation of p21 in p53-deficient tumor cells. Thus, we proposed that alternative administration of TNF-alpha and DOX may be a new and efficient therapeutic strategy for patients that develop resistance to cytotoxic treatment.
    Biochimica et Biophysica Acta 03/2006; 1763(2):182-7. · 4.66 Impact Factor