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  • American Association for Cancer Research (AACR)  (41)
  • Medicine  (41)
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  • Medicine  (41)
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  • 1
    Online Resource
    Online Resource
    Inactivation of Hippo Pathway Is Significantly Associated with Poor Prognosis in Hepatocellular Carcinoma
    American Association for Cancer Research (AACR) ; 2016
    In:  Clinical Cancer Research Vol. 22, No. 5 ( 2016-03-01), p. 1256-1264
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 22, No. 5 ( 2016-03-01), p. 1256-1264
    Abstract: Purpose: The Hippo pathway is a tumor suppressor in the liver. However, the clinical significance of Hippo pathway inactivation in HCC is not clearly defined. We analyzed genomic data from human and mouse tissues to determine clinical relevance of Hippo pathway inactivation in HCC. Experimental Design: We analyzed gene expression data from Mst1/2−/− and Sav1−/− mice and identified a 610-gene expression signature reflecting Hippo pathway inactivation in the liver [silence of Hippo (SOH) signature]. By integrating gene expression data from mouse models with those from human HCC tissues, we developed a prediction model that could identify HCC patients with an inactivated Hippo pathway and used it to test its significance in HCC patients, via univariate and multivariate Cox analyses. Results: HCC patients (National Cancer Institute cohort, n = 113) with the SOH signature had a significantly poorer prognosis than those without the SOH signature [P & lt; 0.001 for overall survival (OS)]. The significant association of the signature with poor prognosis was further validated in the Korean (n = 100, P = 0.006 for OS) and Fudan University cohorts (n = 242, P = 0.001 for OS). On multivariate analysis, the signature was an independent predictor of recurrence-free survival (HR, 1.6; 95% confidence interval, 1.12–2.28: P = 0.008). We also demonstrated significant concordance between the SOH HCC subtype and the hepatic stem cell HCC subtype that had been identified in a previous study (P & lt; 0.001). Conclusions: Inactivation of the Hippo pathway in HCC is significantly associated with poor prognosis. Clin Cancer Res; 22(5); 1256–64. ©2015 AACR.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.CCR-15-1447
    RVK:
    XA 36791
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2016
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  • 2
    Online Resource
    Online Resource
    Abstract 4895: Caveolin-1 modulates docetaxel activity by inducing p53 expression in breast cancer.
    American Association for Cancer Research (AACR) ; 2012
    In:  Cancer Research Vol. 72, No. 8_Supplement ( 2012-04-15), p. 4895-4895
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 72, No. 8_Supplement ( 2012-04-15), p. 4895-4895
    Abstract: Caveolin-1 is reported to be down-regulated in breast cancers compared with normal mammary tissue. More recent data showed that high caveolin-1 expression is more associated with basaloid cancers than ER and/or PR or HER-2 expressing cancers. Investigatirs have reported that Caveolin-1 promoted resistance to chemotherapy-induced apoptosis in Ewing's sarcoma cells. However, the biologic relevance of caveolin-1 in breast cancer remains unclear. Thus, the aim of this study is to investigate its potential biologic relevance of Caveolin-1 to cell survival after docetaxel chemotherapy, one of the most important drug in breast cancer treatment. In this current study, we first showed that Caveolin-1 protein expression was suppressed in the ER(+) human breast cancer cell lines (MCF-7, T47D, and ZR75-1), but not in triple negative cancer cells (MDA-MB-231 and HS578T) and one of the HER-2 type cell (HCC1954) using Western blot analysis. Better cytotoxic effect of docetaxel was observed in the caveolin-1-expressing triple negative cells and HER-2 type cell than the other caveolin-1-deficient HER-2 type and luminal type of cancer cells. Next, caveolin-1 gene was reintroduced into caveolin-1 deficient luminal type breast cancer cells (MCF-7 and ZR75-1) to investigate its potential modulatory effect on docetaxel-induced cytotoxicity. The cell proliferation and MTT assay showed that the overexpressed caveolin-1 had further modulated docetaxel-induced anti-proliferative and cytotoxic effect in the luminal type cells. The anti-proliferative effect of docetaxel in the caveolin-1 gene over-expressed breast cancer cell lines was accompanied by decreasing cyclin D1 expression and inducing cyclin B1 accumulation, then resulting in cell cycle arrest at G2/M phase in the FACS analysis. In addition, re-introduction of caveolin-1 further increased docetaxel-induced cell death by synergistically inducing p53 expression and subsequent induction of p21, then finally apoptosis of breast cancer cells. These results were verified in the mouse model using SCID mice implated with either Caveolin-1-MCF-7 cells or control MCF-7 cells. When each group of tumor-bearing mice were treated by docetacel, mice with Caveolin-1-MCF-7 tumors showed a signiflcantly smaller tumors than those of control group. These results suggest that caveolin-1 may have a modulating factor for docetaxel activity by inducing p53 expression in breast cancer patients. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 4895. doi:1538-7445.AM2012-4895
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2012-4895
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2012
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  • 3
    Online Resource
    Online Resource
    Gene Expression–Based Recurrence Prediction of Hepatitis B Virus–Related Human Hepatocellular Carcinoma
    American Association for Cancer Research (AACR) ; 2008
    In:  Clinical Cancer Research Vol. 14, No. 7 ( 2008-04-01), p. 2056-2064
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 14, No. 7 ( 2008-04-01), p. 2056-2064
    Abstract: Purpose: The poor prognosis of hepatocellular carcinoma (HCC) is, in part, due to the high rate of recurrence even after “curative resection” of tumors. Therefore, it is axiomatic that the development of an effective prognostic prediction model for HCC recurrence after surgery would, at minimum, help to identify in advance those who would most benefit from the treatment, and at best, provide new therapeutic strategies for patients with a high risk of early recurrence. Experimental Design: For the prediction of the recurrence time in patients with HCC, gene expression profiles were generated in 65 HCC patients with hepatitis B infections. Result: Recurrence-associated gene expression signatures successfully discriminated between patients at high-risk and low-risk of early recurrence (P = 1.9 × 10−6, log-rank test). To test the consistency and robustness of the recurrence signature, we validated its prognostic power in an independent HCC microarray data set. CD24 was identified as a putative biomarker for the prediction of early recurrence. Genetic network analysis suggested that SP1 and peroxisome proliferator–activated receptor-α might have regulatory roles for the early recurrence of HCC. Conclusion: We have identified a gene expression signature that effectively predicted early recurrence of HCC independent of microarray platforms and cohorts, and provided novel biological insights into the mechanisms of tumor recurrence.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.CCR-07-1473
    RVK:
    XA 36791
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2008
    detail.hit.zdb_id: 1225457-5
    detail.hit.zdb_id: 2036787-9
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  • 4
    Online Resource
    Online Resource
    Gene Expression Signature–Based Prognostic Risk Score in Gastric Cancer
    American Association for Cancer Research (AACR) ; 2011
    In:  Clinical Cancer Research Vol. 17, No. 7 ( 2011-04-01), p. 1850-1857
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 17, No. 7 ( 2011-04-01), p. 1850-1857
    Abstract: Purpose: Despite continual efforts to develop a prognostic model of gastric cancer by using clinical and pathologic parameters, a clinical test that can discriminate patients with good outcomes from those with poor outcomes after gastric cancer surgery has not been established. We aim to develop practical biomarker-based risk score that can predict relapse of gastric cancer after surgical treatment. Experimental Design: Microarray technologies were used to generate and analyze gene expression profiling data from 65 gastric cancer patients to identify biomarker genes associated with relapse. The association of expression patterns of identified genes with relapse and overall survival was validated in independent gastric cancer patients. Results: We uncovered two subgroups of gastric cancer that were strongly associated with the prognosis. For the easy translation of our findings into practice, we developed a scoring system based on the expression of six genes that predicted the likelihood of relapse after curative resection. In multivariate analysis, the risk score was an independent predictor of relapse in a cohort of 96 patients. We were able to validate the robustness of the six-gene signature in an additional independent cohort. Conclusions: The risk score derived from the six-gene set successfully prognosticated the relapse of gastric cancer patients after gastrectomy. Clin Cancer Res; 17(7); 1850–7. ©2011 AACR.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.CCR-10-2180
    RVK:
    XA 36791
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2011
    detail.hit.zdb_id: 1225457-5
    detail.hit.zdb_id: 2036787-9
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  • 5
    Online Resource
    Online Resource
    Abstract 413: Overexpression of Snail is associated with lymph node metastasis and poor prognosis in patients with gastric cancer.
    American Association for Cancer Research (AACR) ; 2013
    In:  Cancer Research Vol. 73, No. 8_Supplement ( 2013-04-15), p. 413-413
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 73, No. 8_Supplement ( 2013-04-15), p. 413-413
    Abstract: Background: Epithelial-mesenchymal transition (EMT) plays a significant role in tumor progression and invasion. Snail is a known regulator of EMT in various malignant tumors. This study investigated the role of Snail in gastric cancer. Methods: We examined the effects of silenced or overexpressed Snail using lenti-viral constructs in gastric cancer cells. Immunohistochemical analysis of tissue microarrays from 314 patients with gastric adenocarcinoma (GC) was used to determine Snail's clinicopathological and prognostic significance. Differential gene expression in 45 GC specimens with Snail overexpression was investigated using cDNA microarray analysis. Results: Silencing of Snail by shRNA decreased invasion and migration in GC cell lines. Conversely, Snail overexpression increased invasion and migration of gastric cancer cells, in line with increased VEGF and MMP11. Snail overexpression (≥75% positive nuclear staining) was also significantly associated with tumor progression (P & lt; 0.001), lymph node metastases (P = 0.002), lymphovascular invasion (P = 0.002), and perineural invasion (P = 0.002) in the 314 GC patients, and with shorter survival (P = 0.023). cDNA microarray analysis revealed 213 differentially expressed genes in GC tissues with Snail overexpression, including genes related to metastasis and invasion. Conclusion: Snail significantly affects invasiveness/migratory ability of GCs, and may also be used as a predictive biomarker for prognosis or aggressiveness of GCs. Citation Format: Chae Hwa Kwon, Na Ri Shin, Eun Hui Jeong, Chang In Choi, Hyun Jung Moon, In Sun Chu, Gwang Ha Kim, Tae Yong Jeon, Jae Hyuk Lee, Do Youn Park. Overexpression of Snail is associated with lymph node metastasis and poor prognosis in patients with gastric cancer. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 413. doi:10.1158/1538-7445.AM2013-413
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2013-413
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2013
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    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 6
    Online Resource
    Online Resource
    Wnt/β-Catenin Small-Molecule Inhibitor CWP232228 Preferentially Inhibits the Growth of Breast Cancer Stem-like Cells
    American Association for Cancer Research (AACR) ; 2015
    In:  Cancer Research Vol. 75, No. 8 ( 2015-04-15), p. 1691-1702
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 75, No. 8 ( 2015-04-15), p. 1691-1702
    Abstract: Breast cancer stem cells (BCSC) are resistant to conventional chemotherapy and radiotherapy, which may destroy tumor masses but not all BCSC that can mediate relapses. In the present study, we showed that the level of Wnt/β-catenin signaling in BCSC is relatively higher than in bulk tumor cells, contributing to a relatively higher level of therapeutic resistance. We designed a highly potent small-molecule inhibitor, CWP232228, which antagonizes binding of β-catenin to T-cell factor (TCF) in the nucleus. Notably, although CWP232228 inhibited the growth of both BCSC and bulk tumor cells by inhibiting β-catenin–mediated transcription, BCSC exhibited greater growth inhibition than bulk tumor cells. We also documented evidence of greater insulin-like growth factor-I (IGF-I) expression by BCSC than by bulk tumor cells and that CWP232228 attenuated IGF-I–mediated BCSC functions. These results suggested that the inhibitory effect of CWP232228 on BCSC growth might be achieved through the disruption of IGF-I activity. Taken together, our findings indicate that CWP232228 offers a candidate therapeutic agent for breast cancer that preferentially targets BCSC as well as bulk tumor cells. Cancer Res; 75(8); 1691–702. ©2015 AACR.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/0008-5472.CAN-14-2041
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2015
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    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 7
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    Online Resource
    Abstract 1768: Enhanced cytotoxicity and apoptosis of cisplatin by p53-reactivating small molecule RITA in head and neck cancer
    American Association for Cancer Research (AACR) ; 2012
    In:  Cancer Research Vol. 72, No. 8_Supplement ( 2012-04-15), p. 1768-1768
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 72, No. 8_Supplement ( 2012-04-15), p. 1768-1768
    Abstract: Overexpression of MDM2 inactivates the tumor suppressive function of p53 and a small-molecule reactivation of p53 and induction of tumor cell apoptosis (RITA) disrupts the MDM2-p53 interaction. We evaluated whether the restoration of p53 function by RITA enhances cytotoxicity and apoptosis of cisplatin in head-and-neck cancer (HNC). RITA was tested in four human HNC cell lines differing in TP53 status. In vitro and in vivo growth suppression, cell cycle arrest, apoptosis after RITA treatment individually or in combination with cisplatin were assessed. RITA induced prominent accumulation and reactivation of p53 in a wild-type TP53-bearing tumor cell line. RITA showed maximal growth suppression in tumor cells showing MDM2-dependent p53 degradation. RITA upregulated p21, BAX, and cleavage of caspase-3 but the p53-dependent apoptosis was blocked by pifithrin-μ. Strong induction of apoptosis rather than G2-phase arrest was observed along with increased dose of RITA. In combination therapy, RITA enhanced the growth inhibition and apoptosis of HNC by cisplatin in vitro and in vivo. Our data suggest that the restoration of p53 tumor suppressive function by RITA enhances cytotoxicity and apoptosis of cisplatin, which may offer an attractive strategy for treating HNC. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1768. doi:1538-7445.AM2012-1768
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2012-1768
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2012
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 8
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    Expression Signature Defined by FOXM1–CCNB1 Activation Predicts Disease Recurrence in Non–Muscle-Invasive Bladder Cancer
    American Association for Cancer Research (AACR) ; 2014
    In:  Clinical Cancer Research Vol. 20, No. 12 ( 2014-06-15), p. 3233-3243
    Details
    In: Clinical Cancer Research, American Association for Cancer Research (AACR), Vol. 20, No. 12 ( 2014-06-15), p. 3233-3243
    Abstract: Purpose: Although standard treatment with transurethral resection and intravesical therapy (IVT) is known to be effective to address the clinical behavior of non–muscle-invasive bladder cancer (NMIBC), many patients fail to respond to the treatment and frequently experience disease recurrence. Here, we aim to identify a prognostic molecular signature that predicts the NMIBC heterogeneity and response to IVT. Experimental Design: We analyzed the genomic profiles of 102 patients with NMIBC to identify a signature associated with disease recurrence. The validity of the signature was verified in three independent patient cohorts (n = 658). Various statistical methods, including a leave-one-out cross-validation and multivariate Cox regression analyses, were applied to identify a signature. We confirmed an association between the signature and tumor aggressiveness with experimental assays using bladder cancer cell lines. Results: Gene expression profiling in 102 patients with NMIBC identified a CCNB1 signature associated with disease recurrence, which was validated in another three independent cohorts of 658 patients. The CCNB1 signature was shown to be an independent risk factor by a multivariate analysis and subset stratification according to stage and grade [HR, 2.93; 95% confidence intervals (CI), 1.302–6.594; P = 0.009]. The subset analysis also revealed that the signature could identify patients who would benefit from IVT. Finally, gene network analyses and experimental assays indicated that NMIBC recurrence could be mediated by FOXM1–CCNB1–Fanconi anemia pathways. Conclusions: The CCNB1 signature represents a promising diagnostic tool to identify patients with NMIBC who have a high risk of recurrence and to predict response to IVT. Clin Cancer Res; 20(12); 3233–43. ©2014 AACR.
    Type of Medium: Online Resource
    ISSN: 1078-0432 , 1557-3265
    URL: Article
    DOI: 10.1158/1078-0432.CCR-13-2761
    RVK:
    XA 36791
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2014
    detail.hit.zdb_id: 1225457-5
    detail.hit.zdb_id: 2036787-9
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  • 9
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    Abstract 3830: E2F1-FOXM1 activation predicts progression of non-muscle invasive bladder cancer
    American Association for Cancer Research (AACR) ; 2014
    In:  Cancer Research Vol. 74, No. 19_Supplement ( 2014-10-01), p. 3830-3830
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 74, No. 19_Supplement ( 2014-10-01), p. 3830-3830
    Abstract: Backgrounds: Bladder cancer is a genetic disorder driven by the accumulative changes of the multiple genes, such as E2F1, FOXM1, and EZH2. The objective of this study is to estimate a prognostic value of gene expression signature and identify putative signaling pathway for mediating progression of non-muscle invasive bladder cancer (NMIBC). Methods: Gene expression profiling was performed using primary NMIBC cohort to identify a signature correlated with disease progression. The signature was validated in three independent cohorts. The association between the signature and prognosis of NMIBC patients was assessed using various statistical methods including a leave-one-out cross-validation and multivariate Cox regression analyses. The upstream regulator analysis of the genes in the signature was performed by Ingenuity Pathway Analysis TM. We also confirmed a prognostic relevance of the signature with experimental assays using bladder cancer cell lines. Results: Kaplan-Meier analysis in the discovery cohort revealed significant differences in disease progression associated with the expression signature of E2F1-associated genes (p = 0.003), which produced consistent prognostic pattern in the validation cohorts. Multivariate Cox regression analysis revealed that the signature was an independent strong predictor of disease progression (hazard ratio = 6.082, 95% confidence interval = 3.280 to 11.279, p & lt; 0.001). In subset analyses, the signature could identify patients who would benefit from intravesical immunotherapy. Lastly, upstream regulator analyses and experimental assays of the signature revealed that NMIBC progression could be mediated by E2F1-FOXM1 pathways. Conclusion: The prognostic molecular signature defined by activation of E2F1 and FOXM1 represents a promising diagnostic tool to identify high risk NMIBC patients. Citation Format: Seon-Kyu Kim, Se-Ra Lee, Yun-Gil Roh, Bicna Song, Kiejung Park, Sun-Hee Leem, In-Sun Chu. E2F1-FOXM1 activation predicts progression of non-muscle invasive bladder cancer. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 3830. doi:10.1158/1538-7445.AM2014-3830
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2014-3830
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2014
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 10
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    Abstract 3348: Inhibition of MDMX by XI-011 induces p53-mediated apoptosis in head and neck cancer.
    American Association for Cancer Research (AACR) ; 2013
    In:  Cancer Research Vol. 73, No. 8_Supplement ( 2013-04-15), p. 3348-3348
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 73, No. 8_Supplement ( 2013-04-15), p. 3348-3348
    Abstract: Overexpression of MDM2 or MDMX inactivates the tumor-suppressive function of p53. Restoration of p53 function counteracting these p53 repressors can lead to in vivo tumor regression. Therefore, we evaluated whether the restoration of p53 function by a small-molecule p53 activator XI-011, a pseudouria derivative NSC146109, induce apoptosis in head-and-neck cancer (HNC). The effects of XI-011 treatment in four HNC cell lines were tested, individually or in combination with nutlin-3a, an inhibitor of MDM2-p53 interactions, and its growth suppression, cell-cycle arrest, and apoptosis were assessed. XI-011 induced accumulation and reactivation of p53 in a wild-type TP53-bearing HNC cell line. XI-011 showed maximal growth suppression in tumor cells with overexpression of MDMX and MDMX-dependent p53 degradation. With down-regulation of MDMX mRNA and protein levels, XI-011 upregulated expression of p21 and proapoptotic genes and promoted apoptosis in a dose-dependent manner. Notably, the apoptotic response was blocked by inhibition of p53 or MDMX gene expression, demonstrating the p53 and MDMX dependence of XI-011 effects. XI-011 decreased the viability of HNC cells expression low levels of MDMX in a less-efficient manner. Interestingly, in combination therapy, XI-011 synergistically acted with nutlin-3a to inhibit growth of HNC cells. Our data suggest that the MDMX inhibition and p53 functional restoration by XI-011 effectively induced cytotoxicity and apoptosis in cancer cells, an action that may offer a promising strategy for treating HNC. Citation Format: In Sun Ryu, Chang Hwan Ryu, Hyun Bae Park, Eunhye Kim, Jong-Lyel Roh. Inhibition of MDMX by XI-011 induces p53-mediated apoptosis in head and neck cancer. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 3348. doi:10.1158/1538-7445.AM2013-3348
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2013-3348
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2013
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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