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  • Wang, Xianghong  (11)
  • 2005-2009  (11)
  • 1
    Online Resource
    Online Resource
    MAD2 expression and its significance in mitotic checkpoint control in testicular germ cell tumour
    Elsevier BV ; 2007
    In:  Biochimica et Biophysica Acta (BBA) - Molecular Cell Research Vol. 1773, No. 6 ( 2007-06), p. 821-832
    Details
    In: Biochimica et Biophysica Acta (BBA) - Molecular Cell Research, Elsevier BV, Vol. 1773, No. 6 ( 2007-06), p. 821-832
    Type of Medium: Online Resource
    ISSN: 0167-4889
    URL: Article
    DOI: 10.1016/j.bbamcr.2007.03.014
    RVK:
    WA 15000
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2007
    detail.hit.zdb_id: 2209512-3
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    Id-1 Induces Proteasome-dependent Degradation of the HBX Protein
    Elsevier BV ; 2008
    In:  Journal of Molecular Biology Vol. 382, No. 1 ( 2008-09), p. 34-43
    Details
    In: Journal of Molecular Biology, Elsevier BV, Vol. 382, No. 1 ( 2008-09), p. 34-43
    Type of Medium: Online Resource
    ISSN: 0022-2836
    URL: Article
    DOI: 10.1016/j.jmb.2007.06.020
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2008
    detail.hit.zdb_id: 1355192-9
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    Inactivation of Human MAD2B in Nasopharyngeal Carcinoma Cells Leads to Chemosensitization to DNA-Damaging Agents
    American Association for Cancer Research (AACR) ; 2006
    In:  Cancer Research Vol. 66, No. 8 ( 2006-04-15), p. 4357-4367
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 66, No. 8 ( 2006-04-15), p. 4357-4367
    Abstract: Rev7p has been suggested to play an important role in regulating DNA damage response in yeast, and recently, the human homologue (i.e., MAD2B) has been identified, which shares significant homology to the mitotic checkpoint protein MAD2. In this study, we investigated whether MAD2B played a key role in cellular sensitivity to DNA-damaging anticancer drugs by suppressing its expression using RNA interference in nasopharyngeal carcinoma cells. Using colony formation assay, we found that suppression of MAD2B conferred hypersensitivity to a range of DNA-damaging agents, especially DNA cross-linkers, such as cisplatin, and γ-irradiation. This effect was associated with reduced frequencies of spontaneous and drug-induced mutations, elevated phosphorylation of histone H2AX, and markedly increased chromosomal aberrations in response to DNA damage. In addition, there was also a significant decrease in cisplatin-induced sister chromatid exchange rate, a marker for homologous recombination-mediated post-replication repair in MAD2B-depleted cells. These results indicate that MAD2B may be a key factor in regulating cellular response to DNA damage in cancer cells. Our findings reveal a novel strategy for cancer therapy, in which cancer cells are sensitized to DNA-damaging anticancer drugs through inactivation of the MAD2B gene. (Cancer Res 2006; 66(8): 4357-67)
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-05-3602
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2006
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 4
    Online Resource
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    Id‐1 promotes tumorigenicity and metastasis of human esophageal cancer cells through activation of PI3K/AKT signaling pathway
    Wiley ; 2009
    In:  International Journal of Cancer Vol. 125, No. 11 ( 2009-12), p. 2576-2585
    Details
    In: International Journal of Cancer, Wiley, Vol. 125, No. 11 ( 2009-12), p. 2576-2585
    Abstract: Id‐1 (inhibitor of differentiation or DNA binding) is a helix‐loop‐helix protein that is overexpressed in many types of cancer including esophageal squamous cell carcinoma (ESCC). We previously reported that ectopic Id‐1 expression activates the phosphatidylinositol‐3‐kinase (PI3K)/protein kinase B (AKT) signaling pathway in human esophageal cancer cells. In this study, we confirmed a positive correlation between Id‐1 and phospho‐AKT (Ser473) expressions in ESCC cell lines, as well as in ESCC on a tissue microarray. To investigate the significance of Id‐1 in esophageal cancer progression, ESCC cells with stable ectopic Id‐1 expression were inoculated subcutaneously into the flank of nude mice and were found to form larger tumors that showed elevated Ki‐67 proliferation index and increased angiogenesis, as well as reduced apoptosis, compared with control cells expressing the empty vector.The Id‐1‐overexpressing cells also exhibited enhanced metastatic potential in the experimental metastasis assay. Treatment with the PI3K inhibitor LY294002 attenuated the tumor promotion effects of Id‐1, indicating that the effects were mediated by the PI3K/AKT signaling pathway. In addition, our in vitro experiments showed that ectopic Id‐1 expression altered the expression levels of markers associated with epithelial–mesenchymal transition and enhanced the migration ability of esophageal cancer cells. The Id‐1‐overexpressing ESCC cells also exhibited increased invasive potential, which was in part due to PI3K/AKT‐dependent modulation of matrix metalloproteinase‐9 expression. In conclusion, our results provide the first evidence that Id‐1 promotes tumorigenicity and metastasis of human esophageal cancer in vivo and that the PI3K inhibitor LY294002 can attenuate these effects. © 2009 UICC
    Type of Medium: Online Resource
    ISSN: 0020-7136 , 1097-0215
    URL: Issue
    URL: Article
    DOI: 10.1002/ijc.v125:11
    DOI: 10.1002/ijc.24675
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 2009
    detail.hit.zdb_id: 218257-9
    detail.hit.zdb_id: 1474822-8
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  • 5
    Online Resource
    Online Resource
    CDC25A Functions as a Novel Ar Corepressor in Prostate Cancer Cells
    Elsevier BV ; 2009
    In:  Journal of Molecular Biology Vol. 385, No. 2 ( 2009-01), p. 446-456
    Details
    In: Journal of Molecular Biology, Elsevier BV, Vol. 385, No. 2 ( 2009-01), p. 446-456
    Type of Medium: Online Resource
    ISSN: 0022-2836
    URL: Article
    DOI: 10.1016/j.jmb.2008.10.070
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2009
    detail.hit.zdb_id: 1355192-9
    SSG: 12
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  • 6
    Online Resource
    Online Resource
    Id‐1 promotes proliferation of p53‐deficient esophageal cancer cells
    Wiley ; 2006
    In:  International Journal of Cancer Vol. 119, No. 3 ( 2006-08), p. 508-514
    Details
    In: International Journal of Cancer, Wiley, Vol. 119, No. 3 ( 2006-08), p. 508-514
    Abstract: The helix‐loop‐helix protein inhibitor of differentiation and DNA binding (Id‐1) is known to promote cellular proliferation in several types of human cancer. Although it has been reported that Id‐1 is over‐expressed in esophageal squamous cell carcinoma (ESCC), its function and signaling pathways in esophageal cancer are unknown. In our study, we investigated the direct effects of Id‐1 on esophageal cancer cell growth by transfecting an Id‐1 expression vector into an ESCC cell line (HKESC‐3), which showed serum‐dependent Id‐1 expression. Ectopic Id‐1 expression resulted in increased serum‐independent cell growth and G1‐S phase transition, as well as up‐regulation of mouse double minute 2 (MDM2) and down‐regulation of p21 Waf1/Cip1 protein expressions in the transfectant clones in a p53‐independent manner. However, overexpression of Id‐1 had no effect on the pRB, CDK4 and p16 INK4A expressions. Stable transfection of Id‐1 antisense expression vector to inhibit the expression of endogenous Id‐1 in another ESCC cell line (HKESC‐1) reversed the effects on MDM2 and p21 Waf1/Cip1 . In addition, Id‐1 expression protected ESCC cells from Tumor Necrosis Factor (TNF)‐α‐induced apoptosis by up‐regulating and activating Bcl‐2. In conclusion, our study provides evidence for the first time that Id‐1 plays a role in both proliferation and survival of esophageal cancer cells. Our findings also suggest that unlike prostate, hepatocellular and nasopharyngeal carcinomas in which Id‐1 induces cell proliferation through inactivation of p16 INK4A /RB pathway, the increased cell proliferation observed in ESCC cells may be mediated through a different mechanism. © 2006 Wiley‐Liss, Inc.
    Type of Medium: Online Resource
    ISSN: 0020-7136 , 1097-0215
    URL: Issue
    URL: Article
    DOI: 10.1002/ijc.v119:3
    DOI: 10.1002/ijc.21874
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 2006
    detail.hit.zdb_id: 218257-9
    detail.hit.zdb_id: 1474822-8
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  • 7
    Online Resource
    Online Resource
    Epigenetic inactivation of CHFR in nasopharyngeal carcinoma through promoter methylation
    Wiley ; 2005
    In:  Molecular Carcinogenesis Vol. 43, No. 4 ( 2005-08), p. 237-245
    Details
    In: Molecular Carcinogenesis, Wiley, Vol. 43, No. 4 ( 2005-08), p. 237-245
    Abstract: Chromosomal instability (CIN) is a cytogenetic hallmark of human cancers. Increasing evidence suggests that impairment of mitotic checkpoint is causally associated with CIN. CHFR is one of the mitotic checkpoint regulators and it delays chromosome condensation in response to mitotic stress. Epigenetic inactivation of CHFR through promoter CpG hypermethylation may lead to CIN and has been reported in several human cancers. In this study, we investigated the CHFR gene expression in a panel of nasopharyngeal carcinoma (NPC), prostate, ovarian, and breast cancer cell lines. We found that the expression of CHFR mRNA was significantly decreased or undetectable in all eight NPC cell lines as well as three human NPC xenografts, whereas non‐malignant nasopharyngeal cell lines and other cancer cell lines tested expressed CHFR at relatively high levels. Hypermethylation of CHFR promoter region was also strongly correlated with decreased CHFR expression in NPC cell lines and xenografts. Treatment with a methyltransferase inhibitor, 5‐aza‐2′‐deoxycytidine, led to restoration of CHFR expression in NPC cell lines. More importantly, hypermethylation of CHFR promoter region was detected in 61.1% (22 out of 36) of primary NPC tumors while it was absent in non‐malignant tissues. These findings suggest that downregulation of CHFR is a common event in NPC cells which may be due to hypermethylation of the gene promoter region. © 2005 Wiley‐Liss, Inc.
    Type of Medium: Online Resource
    ISSN: 0899-1987 , 1098-2744
    URL: Issue
    URL: Article
    DOI: 10.1002/mc.v43:4
    DOI: 10.1002/mc.20106
    Language: English
    Publisher: Wiley
    Publication Date: 2005
    detail.hit.zdb_id: 2001984-1
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  • 8
    Online Resource
    Online Resource
    Id‐1 modulates senescence and TGF‐β1 sensitivity in prostate epithelial cells
    Wiley ; 2006
    In:  Biology of the Cell Vol. 98, No. 9 ( 2006-09), p. 523-533
    Details
    In: Biology of the Cell, Wiley, Vol. 98, No. 9 ( 2006-09), p. 523-533
    Abstract: Background information . Loss of sensitivity to TGF‐β1 (transforming growth factor β1)‐induced growth arrest is an important step towards malignant transformation in human epithelial cells, and Id‐1 (inhibitor of differentiation or DNA binding‐1) has been associated with cell proliferation and cell‐cycle progression. Here, we investigated the role of Id‐1 in cellular sensitivity to TGF‐β1. Results . Using an immortalized prostate epithelial cell line, NPTX cells, we suppressed Id‐1 expression through antisense strategy. We found that inhibition of Id‐1 expression suppressed cell proliferation and at the same time induced cellular senescence and G 2 /M cell‐cycle arrest. In addition, inactivation of Id‐1 made cells more vulnerable to TGF‐β1‐induced growth arrest. The sensitization effect on TGF‐β1 was associated with up‐regulation of two downstream effectors of the TGF‐β1 pathway, p21 WAF1/Cip1 and p27 KIP1 . Conclusion . Our results indicate that endogenous Id‐1 levels might be a crucial factor in the development of resistance to TGF‐β1‐induced growth suppression in human prostate epithelial cells.
    Type of Medium: Online Resource
    ISSN: 0248-4900 , 1768-322X
    URL: Article
    DOI: 10.1042/BC20060026
    Language: English
    Publisher: Wiley
    Publication Date: 2006
    detail.hit.zdb_id: 2011750-4
    SSG: 12
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  • 9
    Online Resource
    Online Resource
    Mitotic Arrest Deficient 2 Expression Induces Chemosensitization to a DNA-Damaging Agent, Cisplatin, in Nasopharyngeal Carcinoma Cells
    American Association for Cancer Research (AACR) ; 2005
    In:  Cancer Research Vol. 65, No. 4 ( 2005-02-15), p. 1450-1458
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 65, No. 4 ( 2005-02-15), p. 1450-1458
    Abstract: Recently, mitotic arrest deficient 2 (MAD2)–mediated spindle checkpoint is shown to induce mitotic arrest in response to DNA damage, indicating overlapping roles of the spindle checkpoint and DNA damage checkpoint. In this study, we investigated if MAD2 played a part in cellular sensitivity to DNA-damaging agents, especially cisplatin, and whether it was regulated through mitotic checkpoint. Using nine nasopharyngeal carcinoma (NPC) cell lines, we found that decreased MAD2 expression was correlated with cellular resistance to cisplatin compared with the cell lines with high levels of MAD2. Exogenous MAD2 expression in NPC cells also conferred sensitivity to DNA-damaging agents especially cisplatin but not other anticancer drugs with different mechanisms of action. The increased cisplatin sensitivity in MAD2 transfectants was associated with mitotic arrest and activation of apoptosis pathway evidenced by the increased mitotic index and apoptosis rate as well as decreased Bcl-2 and Bax ratio and expression of cleaved poly(ADP-ribose) polymerase and caspase 3. Our results indicate that the MAD2-induced chemosensitization to cisplatin in NPC cells is mediated through the induction of mitotic arrest, which in turn activates the apoptosis pathway. Our evidence further confirms the previous hypothesis that spindle checkpoint plays an important part in DNA damage-induced cell cycle arrest and suggests a novel role of MAD2 in cellular sensitivity to cisplatin.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-04-0567
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2005
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 10
    Online Resource
    Online Resource
    Suppression of Androgen-Independent Prostate Cancer Cell Aggressiveness by FTY720: Validating Runx2 as a Potential Antimetastatic Drug Screening Platform
    American Association for Cancer Research (AACR) ; 2009
    In:  Clinical Cancer Research Vol. 15, No. 13 ( 2009-07-01), p. 4322-4335
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 15, No. 13 ( 2009-07-01), p. 4322-4335
    Abstract: Purpose: Previously, FTY720 was found to possess potent anticancer effects on various types of cancer. In the present study, we aimed to first verify the role of Runx2 in prostate cancer progression and metastasis, and, subsequently, assessed if FTY720 could modulate Runx2 expression, thus interfering downstream events regulated by this protein. Experimental Design: First, the association between Runx2 and prostate cancer progression was assessed using localized prostate cancer specimens and mechanistic investigation of Runx2-induced cancer aggressiveness was then carried out. Subsequently, the effect of FTY720 on Runx2 expression and transcriptional activity was investigated using PC-3 cells, which highly expressed Runx2 protein. Last, the involvement of Runx2 in FTY720-induced anticancer effects was evaluated by modulating Runx2 expression in various prostate cancer cell lines. Results: Runx2 nuclear expression was found to be up-regulated in prostate cancer and its expression could be used as a predictor of metastasis in prostate cancer. Further mechanistic studies indicated that Runx2 accelerated prostate cancer aggressiveness through promotion of cadherin switching, invasion toward collagen I, and Akt activation. Subsequently, we found that FTY720 treatment down-regulated Runx2 expression and its transcriptional activity, as well as inhibited its regulated downstream events. More importantly, silencing Runx2 in PC-3 enhanced FTY720-induced anticancer effects as well as cell viability inhibition, whereas overexpressing Runx2 in 22Rv1 that expressed very low endogenous Runx2 protein conferred resistance in the same events. Conclusion: This study provided a novel mechanism for the anticancer effect of FTY720 on advanced prostate cancer, thus highlighting the therapeutic potential of this drug in treating this disease.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.CCR-08-3157
    RVK:
    XA 36791
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2009
    detail.hit.zdb_id: 1225457-5
    detail.hit.zdb_id: 2036787-9
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