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  • 1
    Language: English
    In: BMC cancer, 2019-11-01, Vol.19 (1), p.1030-1030
    Description: The lack of predictive biomarkers or test systems contributes to high failure rates of systemic therapy in metastasized colorectal carcinoma, accounting for a still unfavorable prognosis. Here, we present an ex vivo functional assay to measure drug-response based on a tissue slice culture approach. Tumor tissue slices of hepatic metastases of nine patients suffering from colorectal carcinoma were cultivated for 72 h and treated with different concentrations of the clinically relevant drugs Oxaliplatin, Cetuximab and Pembrolizumab. Easy to use, objective and automated analysis routines based on the Halo platform were developed to measure changes in proliferative activity and the morphometric make-up of the tumor. Apoptotic indices were assessed semiquantitatively. Untreated tumor tissue slices showed high morphological comparability with the original "in vivo"-tumor, preserving proliferation and stromal-tumor interactions. All but one patients showed a dosage dependent susceptibility to treatment with Oxaliplatin, whereas only two patients showed responses to Cetuximab and Pembrolizumab, respectively. Furthermore, we identified possible non-responders to Cetuximab therapy in absence of RAS-mutations. This is the first time to demonstrate feasibility of the tissue slice culture approach for metastatic tissue of colorectal carcinoma. An automated readout of proliferation and tumor-morphometry allows for quantification of drug susceptibility. This strongly indicates a potential value of this technique as a patient-specific test-system of targeted therapy in metastatic colorectal cancer. Co-clinical trials are needed to customize for clinical application and to define adequate read-out cut-off values.
    Subject(s): Liver - pathology ; Cell Proliferation ; Humans ; Biomarkers, Pharmacological ; Cells, Cultured ; Liver Neoplasms - drug therapy ; Cetuximab - pharmacology ; Feasibility Studies ; Neoplasm Metastasis ; Oxaliplatin - pharmacology ; Liver - drug effects ; Antibodies, Monoclonal, Humanized - pharmacology ; Colorectal Neoplasms - drug therapy ; Antineoplastic Agents - pharmacology ; Colorectal Neoplasms - pathology ; Liver Neoplasms - secondary ; Organ Culture Techniques ; Apoptosis ; Ethylenediaminetetraacetic acid ; Prognosis ; Metastasis ; Health aspects ; Analysis ; Colorectal cancer ; Index Medicus ; Ex vivo culture ; Colorectal liver metastases ; Predictive biomarker ; Predictive test system ; CRLM
    ISSN: 1471-2407
    E-ISSN: 1471-2407
    Source: BioMedCentral Open Access
    Source: Academic Search Ultimate
    Source: PubMed Central
    Source: Directory of Open Access Journals
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 2
    Language: English
    In: International journal of cancer, 2017-10-15, Vol.141 (8), p.1643-1653
    Description: Cyclin K plays a critical role in transcriptional regulation as well as cell development. However, the role of Cyclin K in prostate cancer is unknown. Here, we describe the impact of Cyclin K on prostate cancer cells and examine the clinical relevance of Cyclin K as a biomarker for patients with prostate cancer. We show that Cyclin K depletion in prostate cancer cells induces apoptosis and inhibits proliferation accompanied by an accumulation of cells in the G2/M phase. Moreover, knockdown of Cyclin K causes mitotic catastrophe displayed by multinucleation and spindle multipolarity. Furthermore, we demonstrate a Cyclin K dependent regulation of the mitotic kinase Aurora B and provide evidence for an Aurora B dependent induction of mitotic catastrophe. In addition, we show that Cyclin K expression is associated with poor biochemical recurrence‐free survival in patients with prostate cancer treated with an adjuvant therapy. In conclusion, targeting Cyclin K represents a novel, promising anti‐cancer strategy to induce cell cycle arrest and apoptotic cell death through induction of mitotic catastrophe in prostate cancer cells. Moreover, our results indicate that Cyclin K is a putative predictive biomarker for clinical outcome and therapy response for patients with prostate cancer. What's new? Cell cycle progression genes represent a promising source for biomarker discovery in prostate cancer, though little is known about their role in the disease. This study shows in prostate cancer cells that depletion of Cyclin K, a cell cycle regulator, is associated with apoptosis and inhibition of proliferation. The effects of Cyclin K downregulation were linked to Cyclin K dependent and Aurora B‐mediated induction of mitotic catastrophe. In patients treated with adjuvant therapy, Cyclin K expression was associated with reduced biochemical recurrence‐free survival. The results warrant further investigation of Cyclin K as predictive biomarker in prostate cancer.
    Subject(s): apoptosis ; prostate cancer ; mitotic catastrophe ; cyclin K ; aurora B ; Aurora Kinase B - genetics ; Prostatic Neoplasms - metabolism ; Prostatic Neoplasms - pathology ; Aurora Kinase B - metabolism ; Aurora Kinase B - biosynthesis ; Humans ; Cell Proliferation - physiology ; Cyclins - genetics ; Male ; Cyclins - deficiency ; Prostatic Neoplasms - genetics ; Cyclins - metabolism ; Mitosis - physiology ; Cell Cycle - physiology ; Cell Line, Tumor ; Apoptosis - physiology ; Prostate cancer ; Adjuvant treatment ; Cancer ; Apoptosis ; Index Medicus
    ISSN: 0020-7136
    E-ISSN: 1097-0215
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 3
    Language: English
    In: BMC cancer, 2019-07-11, Vol.19 (1), p.681-681
    Description: Competing molecular classification systems have been proposed to complement the TNM staging system for a better prediction of survival in colorectal cancer (CRC). However, validation studies are so far lacking. The aim of this study was to validate and extend previously published molecular classifications of CRC in a large independent cohort of CRC patients. CRC patients were recruited into a population-based cohort study (DACHS). Molecular subtypes were categorized based on three previously published classifications. Cox-proportional hazard models, based on the same set of patients and using the same confounders as reported by the original studies, were used to determine overall, cancer-specific, or relapse-free survival for each subtype. Hazard ratios and confidence intervals, as well as Kaplan-Meier plots were compared to those reported by the original studies. We observed similar patterns of worse survival for the microsatellite stable (MSS)/BRAF-mutated and MSS/KRAS-mutated subtypes in our validation analyses, which were included in two of the validated classifications. Of the two MSI subtypes, one defined by additional presence of CIMP-high and BRAF-mutation and the other by tumors negative for CIMP, BRAF and KRAS-mutations, we could not confirm associations with better prognosis as suggested by one of the classifications. For two of the published classifications, we were able to provide results for additional subgroups not included in the original studies (men, other disease stages, other locations). External validation of three previously proposed classifications confirmed findings of worse survival for CRC patients with MSS subtypes and BRAF or KRAS mutations. Regarding MSI subtypes, other patient characteristics such as stage of the tumor, may influence the potential survival benefit. Further integration of methylation, genetic, and immunological information is needed to develop and validate a comprehensive classification that will have relevance for use in clinical practice.
    Subject(s): Colorectal Neoplasms - epidemiology ; Microsatellite Instability ; Reproducibility of Results ; Prognosis ; Proto-Oncogene Proteins p21(ras) - genetics ; Colorectal Neoplasms - genetics ; Humans ; Kaplan-Meier Estimate ; Male ; Biomarkers, Tumor ; Case-Control Studies ; Colorectal Neoplasms - diagnosis ; Genetic Variation ; Molecular Diagnostic Techniques ; Proto-Oncogene Proteins B-raf - genetics ; Female ; Neoplasm Staging ; Coxsackie and Adenovirus Receptor-Like Membrane Protein - genetics ; Population Surveillance ; Gene mutations ; Analysis ; Colorectal cancer ; Genetic aspects ; Research ; Microsatellite instability ; Diagnosis ; Index Medicus ; Molecular subtypes ; Cancer-specific survival ; External validation
    ISSN: 1471-2407
    E-ISSN: 1471-2407
    Source: BioMedCentral Open Access
    Source: Academic Search Ultimate
    Source: PubMed Central
    Source: Directory of Open Access Journals
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 4
    Language: English
    In: Molecular cancer, 2013-10-10, Vol.12 (1), p.120-120
    Description: Overexpression of Decoy Receptor 3 (DcR3), a soluble member of the tumor necrosis factor receptor superfamily, is a common event in several types of cancer. In renal cell carcinoma (RCC), DcR3 overexpression is associated with lymph node and distant metastasis as well as a poor prognosis. However, the functional role and regulation of DcR3 expression in RCC is so far unknown. Modulation of DcR3 expression by siRNA and ectopic gene expression, respectively, was performed in ACHN and 769-P RCC cell lines. Functional effects of a modulated DcR3 expression were analyzed with regard to migration, invasion, adhesion, clonogenicity, and proliferation. Furthermore, quantitative RT-PCR and immunoblot analyses were performed to evaluate the expression of downstream mediators of DcR3. In further experiments, luciferase assays, quantitative RT-PCR and immunoblot analyses were applied to study the regulation of DcR3 expression in RCC. Additionally, an ex vivo tissue slice culture technique combined with immunohistochemistry was used to study the regulation of DcR3 expression in human RCC specimens. Here, we show that DcR3 promotes adhesion, migration and invasiveness of RCC cells. The DcR3-dependent increase in cellular invasiveness is accompanied with an up-regulation of integrin alpha 4, matrixmetalloproteinase 7 and urokinase plasminogen activator (uPA). Further, we identified a signaling pathway regulating DcR3 expression in RCC. Using in vitro experiments as well as an ex vivo RCC tissue slice culture model, we demonstrate that expression of DcR3 is regulated in a PI3K/AKT-dependent manner involving the transcription factor nuclear factor of activated T-cells (NFAT). Taken together, our results identify DcR3 as a key driver of tumor cell dissemination and suggest DcR3 as a promising target for rational therapy of RCC.
    Subject(s): RNA, Small Interfering - genetics ; Signal Transduction ; Carcinoma, Renal Cell - pathology ; Neoplasm Invasiveness ; Receptors, Tumor Necrosis Factor, Member 6b - metabolism ; Humans ; NFATC Transcription Factors - metabolism ; Gene Expression Regulation, Neoplastic ; Morpholines - pharmacology ; Kidney Neoplasms - metabolism ; Phosphatidylinositol 3-Kinases - antagonists & inhibitors ; Cell Adhesion ; Fibronectins - metabolism ; Gene Knockdown Techniques ; Carcinoma, Renal Cell - metabolism ; HEK293 Cells ; Cell Line, Tumor ; Phosphatidylinositol 3-Kinases - physiology ; Kidney Neoplasms - pathology ; Transcription, Genetic ; Chromones - pharmacology ; Proto-Oncogene Proteins c-akt - metabolism ; Receptors, Tumor Necrosis Factor, Member 6b - genetics ; Cell Movement ; Immunohistochemistry ; Tumor necrosis factor ; Genes ; Development and progression ; Carcinoma, Renal cell ; Metastasis ; T cells ; Gene expression ; Integrins ; Index Medicus ; DcR3 ; AKT ; Research ; Renal cell carcinoma ; NFAT
    ISSN: 1476-4598
    E-ISSN: 1476-4598
    Source: BioMedCentral Open Access
    Source: Academic Search Ultimate
    Source: PubMed Central
    Source: Directory of Open Access Journals
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 5
    Language: English
    In: Cancer cell international, 2016, Vol.16 (1), p.42-42
    Description: Deregulation of miRNA-210 is a common event in several types of cancer. However, increased expression levels in the cancer tissue have been associated with both poor and good prognosis of patients. Similarly, the function of miR-210 with regard to cell growth and apoptosis is still controversial. Overexpression of miR-210 was performed in HCT116, SW480 and SW707 colorectal cancer (CRC) cell lines. Functional effects of a modulated miR-210 expression were analyzed with regard to proliferation, clonogenicity, cell cycle distribution, reactive oxygen species (ROS) generation, and apoptosis. Furthermore, quantitative real time (RT)-PCR and immunoblot analyses were performed to investigate signaling pathways affected by miR-210. We show that in CRC cells miR-210 inhibits clonogenicity and proliferation which was accompanied by an accumulation of cells in the G2/M phase of the cell cycle. Additionally, overexpression of miR-210 results in an increase of ROS generation. Moreover, miR-210 mediated the induction of apoptosis which was associated with an upregulation of pro-apoptotic Bim expression and enhanced processing of Caspase 2. Importantly, inhibition of ROS generation rescued cells from miR-210-induced apoptosis. Taken together, miR-210 induces apoptosis in CRC cells via a ROS-dependent mechanism.
    Subject(s): miR-210 ; Colorectal carcinoma ; Primary Research ; ROS ; Bim ; Apoptosis
    ISSN: 1475-2867
    E-ISSN: 1475-2867
    Source: BioMedCentral Open Access
    Source: Academic Search Ultimate
    Source: PubMed Central
    Source: Directory of Open Access Journals
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 6
    Language: English
    In: Molecular oncology, 2020-02, Vol.14 (2), p.363-372
    Description: Previous studies have reported conflicting results regarding the benefit of administering 5‐FU‐based chemotherapy to colon cancer (CC) patients with microsatellite‐instable (MSI‐high) tumors, and results from stage‐specific analyses are scarce. Patients with stage II or III CC were recruited as part of a population‐based study between 2003 and 2015. The Cox regression models including propensity score weighting were used to calculate hazard ratios and confidence intervals for the association between chemotherapy and cancer‐specific (CSS), relapse‐free (RFS), and overall survival (OS) by stage of disease and MSI status of the tumor. Median follow‐up was 6.2 years. A total of 1010 CC patients were included in the analysis (54% stage II, 46% stage III, 20% MSI‐high). Adjuvant chemotherapy was administered to 48 (8.7%) stage II and 366 (79%) stage III patients. Overall, patients who received adjuvant chemotherapy had better CSS [HR = 0.65 (0.49–0.86)] than those who received surgery alone. Among stage II patients, only 64 (12%) cancer‐related deaths occurred, none of which in MSI‐high patients who received chemotherapy. Patients with MSI‐high tumors who received adjuvant treatment showed better CSS and a tendency toward better RFS compared to MSI‐high patients who did not receive chemotherapy [HRCSS = 0.36 (0.15–0.82), HRRFS = 0.49 (0.22–1.06)]. Patients with microsatellite‐stable (MSS) tumors receiving adjuvant chemotherapy also had significantly better survival [HRCSS = 0.65 (0.48–0.87) and HRRFS = 0.68 (0.52–0.88)]. In this population‐based study including stage II and III CC patients, we observed a survival benefit of adjuvant chemotherapy for both MSS and MSI‐high tumors. Adjuvant chemotherapy seemed to be beneficial among high‐risk stage II patients with MSI‐high tumors. In this population‐based study including colon cancer patients with stage II and III disease, a survival benefit of adjuvant chemotherapy was observed for both microsatellite stability and microsatellite‐instable (MSI)‐high tumors. Adjuvant chemotherapy seemed to also be beneficial for high‐risk stage II patients with MSI‐high tumors.
    Subject(s): adjuvant chemotherapy ; microsatellite instability ; colon cancer ; survival ; Colonic Neoplasms - genetics ; Colonic Neoplasms - mortality ; Prognosis ; Follow-Up Studies ; Colonic Neoplasms - drug therapy ; Humans ; Middle Aged ; Proportional Hazards Models ; Neoplasm Recurrence, Local - drug therapy ; Male ; Microsatellite Instability - drug effects ; Colonic Neoplasms - metabolism ; Fluorouracil - therapeutic use ; Antineoplastic Combined Chemotherapy Protocols - therapeutic use ; Female ; Aged ; Neoplasm Staging ; Chemotherapy, Adjuvant - mortality ; Comorbidity ; Colorectal cancer ; Clinical trials ; Population studies ; Microsatellite instability ; Regression analysis ; Cancer therapies ; Survival ; Patients ; Studies ; Survival analysis ; Chemotherapy ; Colon cancer ; Surgery ; Population ; Tumors ; Index Medicus
    ISSN: 1574-7891
    E-ISSN: 1878-0261
    Source: PubMed Central
    Source: Directory of Open Access Journals
    Source: ProQuest Central
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 7
    Language: English
    In: Translational oncology, 2020-02, Vol.13 (2), p.336-345
    Description: INTRODUCTION: Immune checkpoint inhibitors (ICI) have been approved for patients with clear cell renal cell carcinoma (ccRCC), but not all patients benefit from ICI. One reason is the tumor microenvironment (TME) that has substantial influence on patient's prognosis and therapy response. Thus, we comprehensively analyzed the TME of ccRCC regarding prognostic and predictive properties. METHODS: Tumor-infiltrating CD3-positive T-cells, CD8-positive cytotoxic T-lymphocytes (CTLs), regulatory T-cells, B-cells, plasma cells, macrophages, granulocytes, programmed cell death receptor 1 (PD-1), and its ligand PD-L1 were examined in a large hospital-based series of ccRCC with long-term follow-up information (n = 756) and in another patient collective with information on response to nivolumab therapy (n = 8). Tissue microarray technique and digital image analysis were used. Relationship between immune cell infiltration and tumor characteristics, cancer-specific survival (CSS), or response to ICI was examined. RESULTS: Univariate survival analysis revealed that increased tumor-infiltrating B-cells, T-cells, and PD-1-positive cells were significantly associated with favorable CSS and high levels of intratumoral granulocytes, macrophages, cytotoxic T-cells, and PD-L1 significantly with poor CSS. High CTL or B-cell infiltration and high PD-L1 expression of ccRCC tumor cells qualified as independent prognostic biomarkers for patients' CSS. Significantly higher densities of intratumoral T-cells, CTLs, and PD-1-positive immune cells were observed in ccRCC with response to ICI compared with patients with mixed or no response (CD3: p = 0.003; CD8: p = 0.006; PD-1: p = 0.01). DISCUSSION: This study shows that subsets of tumor-infiltrating leukocytes in the TME and also PD-1/PD-L1 provide prognostic and predictive information for patients with ccRCC.
    Subject(s): Checkpoint inhibitor ; Biomarker ; Renal cell carcinoma ; Immune cell ; Original article
    ISSN: 1936-5233
    E-ISSN: 1936-5233
    Source: PubMed Central
    Source: Directory of Open Access Journals
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 8
    Language: English
    In: The Journal of pathology, 2015-12, Vol.237 (4), p.460-471
    Description: About 40% of clear‐cell renal cell carcinomas (ccRCC) harbour mutations in Polybromo‐1 (PBRM1), encoding the BAF180 subunit of a SWI/SNF chromatin remodelling complex. This qualifies PBRM1 as a major cancer gene in ccRCC. The PBRM1 protein alters chromatin structure and its known functions include transcriptional regulation by controlling the accessibility of DNA and influencing p53 transcriptional activity. Since little is known about the regulation of PBRM1, we studied possible mechanisms and interaction partners involved in the regulation of PBRM1 expression. Activation of p53 in RCC cells resulted in a marked decrease of PBRM1 protein levels. This effect was abolished by siRNA‐mediated down‐regulation of p53, and transcriptional activity was not crucial for p53‐dependent PBRM1 regulation. Pulse‐chase experiments determined post‐translational protein degradation to be the underlying mechanism for p53‐dependent PBRM1 regulation, which was accordingly inhibited by proteasome inhibitors. The effects of p53 activation on PBRM1 expression were confirmed in RCC tissue ex vivo. Our results demonstrate that PBRM1 is a target of p53‐induced proteasomal protein degradation and provide further evidence for the influence of PBRM1 on p53 function in RCC tumour cells. Considering the paramount role of p53 in carcinogenesis and the presumptive impact of PBRM1 in RCC development, this novel regulation mechanism might be therapeutically exploited in the future. Copyright © 2015 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
    Subject(s): kidney ; renal cell carcinoma ; PBRM1 ; TP53 ; protein degradation ; Immunohistochemistry ; Carcinoma, Renal Cell - pathology ; Tissue Array Analysis ; Humans ; Kaplan-Meier Estimate ; Proportional Hazards Models ; Tumor Suppressor Protein p53 - metabolism ; Immunoblotting ; Transcription Factors - biosynthesis ; Kidney Neoplasms - metabolism ; Kidney Neoplasms - mortality ; Carcinoma, Renal Cell - metabolism ; Carcinoma, Renal Cell - mortality ; Transfection ; Nuclear Proteins - biosynthesis ; Polymerase Chain Reaction ; Cell Line, Tumor ; Kidney Neoplasms - pathology ; RNA, Small Interfering ; Gene Expression Regulation, Neoplastic - physiology ; Tumor proteins ; Proteolysis ; Analysis ; Cancer
    ISSN: 0022-3417
    E-ISSN: 1096-9896
    Source: Alma/SFX Local Collection
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  • 9
    Language: English
    In: Translational oncology, 2017-12, Vol.10 (6), p.869-875
    Description: BNIP3 (Bcl-2/adenovirus E1B 19-kDa interacting protein 3) is a BH3-only protein that regulates apoptosis and autophagy. BNIP3 plays also an important role in hypoxia-induced cell response and is regulated by HIF1. Here, we studied a possible association of BNIP3 expression and the prognosis of patients with renal cell carcinomas (RCCs) and examined the functional relevance of BNIP3 in the regulation of cell survival and apoptosis of renal carcinoma cells. BNIP3 expression was determined by immunohistochemistry in RCC tumor tissue samples of 569 patients using a tissue microarray. Functional characterization of BNIP3 in renal carcinoma cells indicates prosurvival effects. In human RCC tumor samples, high cytoplasmic BNIP3 expression was associated with high-grade RCCs and regional lymph node metastasis. BNIP3 expression correlated negatively with disease-specific survival. Multivariate Cox regression analysis retained BNIP3 expression as an independent prognostic factor in patients without distant metastasis. Together, our studies imply that BNIP3 regulates cell survival in RCCs and its expression is an independent prognostic marker in patients with localized RCCs.
    Subject(s): Original article
    ISSN: 1936-5233
    E-ISSN: 1936-5233
    Source: PubMed Central
    Source: Directory of Open Access Journals
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 10
    Language: English
    In: Apoptosis (London), 2012-02, Vol.17 (2), p.187-199
    Description: Treatment with the Bcl-2/Bcl-XL inhibitor ABT-737 is a promising novel strategy to therapeutically induce apoptotic cell death in malignant tumors such as glioblastomas. Although many studies have demonstrated that ABT-737 acts synergistically with chemotherapeutic drugs, the possibility of a combined treatment with ionizing radiation (IR) and ABT-737 has not yet been thoroughly investigated. Similarly, the relationship between p53 function and the pro-apoptotic effects of ABT-737 are still obscure. Here, we demonstrate that IR and ABT-737 synergistically induce apoptosis in glioblastoma cells. The sensitivity to ABT-737-mediated cell death is significantly increased by the IR-dependent accumulation of cells in the G2/M cell cycle phase. Wild type p53 function inhibits the efficacy of a combined IR and ABT-737 treatment via a p21-dependent G1 cell cycle arrest. Moreover, mutant as well as wild type p53 counteract the pro-apoptotic activity of ABT-737 by maintaining the expression levels of the Mcl-1 protein. Thus, p53 regulates the sensitivity to ABT-737 of glioblastoma cells. Our results warrant a further evaluation of a novel combination therapy using IR and ABT-737. The efficacy of such a therapy could be substantially enhanced by Mcl-1-lowering strategies.
    Subject(s): Biochemistry, general ; Mcl-1 ; Ionizing radiation ; Biomedicine ; Bcl-2 inhibitor ; ABT-737 ; Cancer Research ; Oncology ; Cell Biology ; Virology ; Apoptosis ; p53 ; Piperazines - administration & dosage ; RNA, Small Interfering - genetics ; Apoptosis - drug effects ; Apoptosis - radiation effects ; Humans ; Tumor Suppressor Protein p53 - metabolism ; bcl-X Protein - genetics ; Apoptosis - genetics ; Nitrophenols - administration & dosage ; Tumor Suppressor Protein p53 - genetics ; Proto-Oncogene Proteins c-bcl-2 - metabolism ; bcl-X Protein - antagonists & inhibitors ; Myeloid Cell Leukemia Sequence 1 Protein ; Biphenyl Compounds - administration & dosage ; Cell Line, Tumor ; Cyclin-Dependent Kinase Inhibitor p21 - metabolism ; Glioblastoma - metabolism ; Proto-Oncogene Proteins c-bcl-2 - antagonists & inhibitors ; Gene Expression Regulation, Neoplastic - radiation effects ; Gene Expression Regulation, Neoplastic - drug effects ; Proto-Oncogene Proteins c-bcl-2 - genetics ; Sulfonamides - administration & dosage ; Radiation, Ionizing ; Chemotherapy ; Nuclear radiation ; Gliomas ; Cell death ; Oncology, Experimental ; Biochemistry ; Research ; Universities and colleges ; Tumor proteins ; Radiotherapy ; Cancer ; Index Medicus
    ISSN: 1360-8185
    E-ISSN: 1573-675X
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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