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  • 1
    Online-Ressource
    Online-Ressource
    Hand1 overexpression inhibits medulloblastoma metastasis
    Elsevier BV ; 2016
    In:  Biochemical and Biophysical Research Communications Vol. 477, No. 2 ( 2016-08), p. 215-221
    Details
    In: Biochemical and Biophysical Research Communications, Elsevier BV, Vol. 477, No. 2 ( 2016-08), p. 215-221
    Materialart: Online-Ressource
    ISSN: 0006-291X
    URL: Article
    DOI: 10.1016/j.bbrc.2016.06.045
    RVK:
    WA 15000
    Sprache: Englisch
    Verlag: Elsevier BV
    Publikationsdatum: 2016
    ZDB Id: 1461396-7
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 2
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    TRPM3 Exhibits Slight Temperature Sensitivity in the Planar Lipid Bilayer System and Requires the Presence of PIP2
    Elsevier BV ; 2016
    In:  Biophysical Journal Vol. 110, No. 3 ( 2016-02), p. 612a-
    Details
    In: Biophysical Journal, Elsevier BV, Vol. 110, No. 3 ( 2016-02), p. 612a-
    Materialart: Online-Ressource
    ISSN: 0006-3495
    URL: Article
    DOI: 10.1016/j.bpj.2015.11.3268
    Sprache: Englisch
    Verlag: Elsevier BV
    Publikationsdatum: 2016
    ZDB Id: 1477214-0
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 3
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    Abstract 202: STAT1 regulates B7H3 mediated angiogenesis in medulloblastoma
    American Association for Cancer Research (AACR) ; 2019
    In:  Cancer Research Vol. 79, No. 13_Supplement ( 2019-07-01), p. 202-202
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 79, No. 13_Supplement ( 2019-07-01), p. 202-202
    Kurzfassung: B7-H3 (CD276), an immune checkpoint member of the B7/CD28 family, plays a key role in the repression of the immune response by cancer cells. B7-H3 is overexpressed on tumor and tumor-associated cells, making it an interesting therapeutic target. B7-H3 also appears to play a role outside of immune evasion, contributing to the progression of cancer via invasion/migration, angiogenesis, and metastasis. Our previous data has confirmed the presence of B7-H3 in highly aggressive Myc+ medulloblastoma (MB) tumors. Data-mining studies revealed that B7-H3 is correlated with Myc expression in Group 3 and 4 MBs, and is associated with worse patient outcomes. miR-29, a tumor suppressor, has been shown downregulating the expression of B7-H3 in various cancers. We have shown that miR-29 can reduce the angiogenesis abilities of D283 and D425 cells by downregulating B7-H3 in vitro. Subsequent RNA-sequencing analysis of miR-29-transfected D283 cells revealed upregulation of STAT1 activity. Immunoblot analysis and real-time PCR of D283 and D425 cells demonstrated increased expression of p-STAT1, when transfected with miR-29 plasmid. Treatment with all-trans retinoic acid induced p-STAT1 expression, with a concomitant decrease in the expression of B7-H3 and MMP-9. This preliminary data revealed a novel role for STAT1 in potentially regulating B7-H3, and consequently, angiogenesis and metastasis in MB. To date, the role of STAT1 in MB progression has not been fully investigated, and so our results provide a new avenue for developing potential treatments for aggressive MB tumors. Citation Format: Ian J. Purvis, Janardhan Avilala, Maheedhara R. Guda, Sujatha Venkataraman, Rajeev Vibhakar, Andrew J. Tsung, Kiran K. Velpula, Swapna Asuthkar. STAT1 regulates B7H3 mediated angiogenesis in medulloblastoma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 202.
    Materialart: Online-Ressource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2019-202
    RVK:
    XA 36000
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: American Association for Cancer Research (AACR)
    Publikationsdatum: 2019
    ZDB Id: 2036785-5
    ZDB Id: 1432-1
    ZDB Id: 410466-3
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 4
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    Abstract 1165: TRPM8 is avidly targeted for degradation in prostate cancer
    American Association for Cancer Research (AACR) ; 2016
    In:  Cancer Research Vol. 76, No. 14_Supplement ( 2016-07-15), p. 1165-1165
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 76, No. 14_Supplement ( 2016-07-15), p. 1165-1165
    Kurzfassung: Transient receptor potential melastatin 8 (TRPM8) is a cold-sensing receptor and a hallmark Ca2+ channel of the prostate epithelium. The TRPM8 mRNA is overexpressed in early prostate tumors with high androgen levels, while anti-androgen therapy greatly reduces its expression. Thus, androgens, which are at the crossroads of several signaling pathways, appear to be associated with TRPM8-mediated Ca2+ signaling. Although, TRPM8 mRNA levels are upregulated during prostate cancer progression, this upregulation is not adequately translated to the TRPM8 protein levels. We identified that the lower TRPM8 protein abundance and activation in LNCaP cells is associated with increased ubiquitination and loss of TRPM8 from the plasma membrane (PM). The mass-spectrometry analysis of TRPM8, immunoprecipitated from LNCaP cells identified ubiquitin-like modifier-activating enzyme 1 (UBA1). PYR-41, a potent inhibitor of the initial enzyme in the ubiquitination cascade, UBA1, increased TRPM8 activity on the PM of LNCaP cells. Our data indicate that PMTRPM8 plays a protective role in prostate cancer progression accompanied by enhanced activation of p53 and Caspase-9. In addition, we found that the promoter region of trpm8 possesses putative binding sites for p53 and that the overexpression of p53 increased the TRPM8 mRNA levels. Our findings support previous studies that suggest the fine balance between AR and p53 expression that regulates androgen-dependent growth of prostate cancer. Thus, we hypothesize that TRPM8 activity significantly contributes to anti-tumor defense mechanism and may serve as a novel therapeutic target in prostate cancer. Citation Format: Swapna Asuthkar, Eleonora Zakharian. TRPM8 is avidly targeted for degradation in prostate cancer. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 1165.
    Materialart: Online-Ressource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2016-1165
    RVK:
    XA 36000
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: American Association for Cancer Research (AACR)
    Publikationsdatum: 2016
    ZDB Id: 2036785-5
    ZDB Id: 1432-1
    ZDB Id: 410466-3
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 5
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    Abstract 1920: miR-211 directly targets pyruvate dehydrogenase kinase 4 to inhibit cellular growth and glucose metabolism in triple negative breast cancer
    American Association for Cancer Research (AACR) ; 2016
    In:  Cancer Research Vol. 76, No. 14_Supplement ( 2016-07-15), p. 1920-1920
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 76, No. 14_Supplement ( 2016-07-15), p. 1920-1920
    Kurzfassung: Deregulated metabolism and aerobic glycolysis are common to many kinds of tumors including, breast cancers driven by a plethora of transcription factors. One such is hypoxia-inducible factor-1α (HIF-1α) known to drive the expression of glycolytic target genes. Here, we identify PDK4 (pyruvate dehydrogenase kinase 4) as a key regulator of HIF-1α signaling. In triple-negative human breast cancer (TNBC) cell lines, we investigated the contribution of PDK4 and HIF-1α to experimental tumor growth, core glucose metabolism and ionizing radiation effects. When these TNBC cells were exposed to 4, 6 and 8Gy treatment, we observed a linear increase in the expression levels of PDK4 and HIF-1α genes. In this study we also report that miR-211, a microRNA predicted to target PDK4 is suppressed in TNBC patient specimens as evidenced by in situ hybridization analysis. The expression levels of PDK4, HIF-1α and RICTOR were reduced with miR-211 over expression while the levels of PDH and FH were observed to be increased. Further, we observed that miR-211 conjugated to cerium oxide nanoparticles (nanoceria) showed increased cytotoxicity. Similar effects were observed when these TNBCs were treated with 5mM DCA, a potent metabolic inhibitor of PDK. Combinatory suppression of PDK4 and HIF-1α exerted synergistic inhibition of lactate released suggesting of reversal of aerobic glycolysis. Alternatively, TCGA datasets were predictive of patient survival, with a PDK4/miR-211 signature robustly predicting poor patient prognosis. Overall, our findings suggest that combined targeting of PDK4 signaling cascade with miR-211 and DCA in combination specifically regulate core glucose metabolism in TNBC. Citation Format: Maheedhara R. Guda, Swapna Asuthkar, Soumen Das, Sudipta Seal, Andrew J. Tsung, Kiran K. Velpula. miR-211 directly targets pyruvate dehydrogenase kinase 4 to inhibit cellular growth and glucose metabolism in triple negative breast cancer. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 1920.
    Materialart: Online-Ressource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2016-1920
    RVK:
    XA 36000
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: American Association for Cancer Research (AACR)
    Publikationsdatum: 2016
    ZDB Id: 2036785-5
    ZDB Id: 1432-1
    ZDB Id: 410466-3
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 6
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    Immunopathology of galectin-3: an increasingly promising target in COVID-19
    F1000 Research Ltd ; 2020
    In:  F1000Research Vol. 9 ( 2020-9-28), p. 1078-
    Details
    In: F1000Research, F1000 Research Ltd, Vol. 9 ( 2020-9-28), p. 1078-
    Materialart: Online-Ressource
    ISSN: 2046-1402
    URL: Journal
    URL: Article
    DOI: 10.12688/f1000research
    DOI: 10.12688/f1000research.25979.2
    Sprache: Englisch
    Verlag: F1000 Research Ltd
    Publikationsdatum: 2020
    ZDB Id: 2699932-8
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  • 7
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    Abstract 3593: PDK1 is a preferential metabolic target in glioblastoma
    American Association for Cancer Research (AACR) ; 2019
    In:  Cancer Research Vol. 79, No. 13_Supplement ( 2019-07-01), p. 3593-3593
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 79, No. 13_Supplement ( 2019-07-01), p. 3593-3593
    Kurzfassung: Glioblastoma (GBM), the most common adult primary malignant brain tumor, carries a high morbidity and mortality despite therapeutic advances. GBM’s progression is associated with a transition from oxidative phosphorylation to aerobic glycolysis as its main source of energy. Our laboratory recently confirmed that overexpression of pyruvate dehydrogenase kinase isoform 1 (PDK1) positively contributes to GBM progression. Here we report a novel role of mitofusin 1 (MFN1), a mitochondrial outer membrane GTPase that is a key regulator of mitochondrial fusion associated with glycolysis. We have shown that both PDK1 and MFN1 are highly co-expressed in glioblastoma patient specimens. Data obtained from The Cancer Genome Atlas demonstrated a positive correlation between PDK1 and MFN1 mRNA levels and the survival of GBM patients. The data obtained from the subtyped glioma stem cells corroborated with the datamining studies. To directly explore the potential MFN1-PDK1 interplay, we used CRISPR/Cas9 to suppress MFN1 expression in proneural, classical and mesenchymal subtypes of GBM stem cells (CSC). In another experiment, using ChIP assay, we showed that both PDK1 and MFN1 are under the transcriptional control of Myc oncogene. We present evidence that silencing MFN1 regulates altered metabolism in GBM CSC by increasing ROS levels, altering mitochondrial membrane potential, reduced lactate metabolites via NMR spectroscopy. Taken together, our results indicate that combined targeting of PDK1 and MFN1 shift Warburg effect towards oxidative phosphorylation, and may have increased therapeutic potential for glioblastoma patients. Citation Format: Maheedhara R. Guda, Swapna Asuthkar, Andrew J. Tsung, Kiran K. Velpula. PDK1 is a preferential metabolic target in glioblastoma [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 3593.
    Materialart: Online-Ressource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2019-3593
    RVK:
    XA 36000
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: American Association for Cancer Research (AACR)
    Publikationsdatum: 2019
    ZDB Id: 2036785-5
    ZDB Id: 1432-1
    ZDB Id: 410466-3
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 8
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    Abstract 1137: Mitochondrial targeting of EGFR-VIII in temozolomide resistant glioblastoma models
    American Association for Cancer Research (AACR) ; 2015
    In:  Cancer Research Vol. 75, No. 15_Supplement ( 2015-08-01), p. 1137-1137
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 75, No. 15_Supplement ( 2015-08-01), p. 1137-1137
    Kurzfassung: Epidermal growth factor receptor (EGFR) over-expression is the most frequent genetic alteration associated with glioblastoma and has emerged as a highly attractive therapeutic target based on its high frequency of gene amplification and mutation as well as its deregulated cell signaling cascades that drive GBM pathophysiology. The genetic aberration of wtEGFR is often accompanied by the overexpression of a mutant EGFR known as EGFR variant III (EGFRvIII), which is expressed in 30% of GBM tumors. Despite recent innovations, may it be neurosurgical techniques, chemotherapeutics or molecular targeted therapies only few treatments showed promise. Temozolomide (TMZ) is one such and has shown improved survival in GBM when administered with concomitant radiotherapy. However, acquired TMZ chemoresistance occurs in more than 90% of recurrent GBMs. To delineate the mechanisms in the context of TMZ resistance, we generated an aggressive TMZ resistant model by continual exposure of U373 cells constitutively expressing EGFRvIII (U373vIII) to 150uM TMZ for 6 months (U373vIIIR). Our preliminary data showed that dichloroacetic acid (DCA) induced apoptosis and demonstrated reduced cell survival in the context of TMZ resistance. DCA treatment also demonstrated reduced EGFRvIII mitochondrial translocation in U373vIIIR cells. Micro array studies conducted on U373vIII or U373vIIR and their subsequent treatment with DCA revealed that PDK1 is the sole target in TMZ resistant tumors expressing EGFRvIII. Since EGFRvIII expression displays an aggressive phenotype yet remains tumor specific, we propose studying DCA alone or in combination with dasatinib, an inhibitor of EGFR subcellular translocation, in U373vIII and U373vIII-TMZ-R cell lines. By more accurately depicting the status of GBM at the time of recurrence after standard of care chemotherapy treatment, the investigation of DCA will augment and possibly redefine our current understanding of resistance mechanisms and establish novel methods of circumventing this pervasive phenomena. Note: This abstract was not presented at the meeting. Citation Format: Kiran Kumar Velpula, Swapna Asuthkar, Sarah E. Martin, Justin D. Lathia, Andrew J. Tsung. Mitochondrial targeting of EGFR-VIII in temozolomide resistant glioblastoma models. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 1137. doi:10.1158/1538-7445.AM2015-1137
    Materialart: Online-Ressource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2015-1137
    RVK:
    XA 36000
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: American Association for Cancer Research (AACR)
    Publikationsdatum: 2015
    ZDB Id: 2036785-5
    ZDB Id: 1432-1
    ZDB Id: 410466-3
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 9
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    Functional and structural analysis of mice TRPC6 with human analogue through homology modelling
    Inderscience Publishers ; 2014
    In:  International Journal of Bioinformatics Research and Applications Vol. 10, No. 2 ( 2014), p. 206-
    Details
    In: International Journal of Bioinformatics Research and Applications, Inderscience Publishers, Vol. 10, No. 2 ( 2014), p. 206-
    Materialart: Online-Ressource
    ISSN: 1744-5485 , 1744-5493
    URL: Article
    DOI: 10.1504/IJBRA.2014.059536
    Sprache: Englisch
    Verlag: Inderscience Publishers
    Publikationsdatum: 2014
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 10
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    Abstract 576: Gadd45a sensitizes medulloblastoma cells to irradiation and modulates the cellular switch from migratory to stationary cell phase by downregulating MMP-9
    American Association for Cancer Research (AACR) ; 2011
    In:  Cancer Research Vol. 71, No. 8_Supplement ( 2011-04-15), p. 576-576
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 71, No. 8_Supplement ( 2011-04-15), p. 576-576
    Kurzfassung: Gadd45a protein is induced in medulloblastoma cell lines by treatment with ionizing radiation (IR), which requires p53 stabilization. The role of Gadd45a in IR-induced G2-M arrest of medulloblastoma cells is demonstrated by its increased binding to Cdc2, thereby inactivating Cdc2 kinase activity. Knockdown of Gadd45a alleviates G2-M blockage and results in decreased binding of Gadd45a to Cdc2. Further, the anti-tumorigenic role of Gadd45a is mediated by the negative regulation of β-catenin and its nuclear translocation, which might decrease the β-catenin/LEF-1-mediated transactivation of cell invasion proteins, such as MMP-9, examined in the present study. Overexpression of Gadd45a protein with IR treatment resulted in decreased nuclear levels of β-catenin, increased cytoplasmic levels of p-β-catenin, and increased distribution of β-catenin on membrane E and N-cadherins. The IR-treated control cells showed contrary results with demonstrated loss of E-cadherin, gain of N-cadherin, and inhibition of β-catenin binding to membrane cadherins as well as increased nuclear translocation of β-catenin. Zymography studies demonstrate the negative regulation of IR-induced MMP-9 activity by Gadd45a overexpression. Wound healing and Matrigel invasion assays confirmed the anti-tumorigenic and anti-metastatic role of Gadd45a in medulloblastoma cell lines. Furthermore, siRNA-mediated knockdown of MMP-9 results in prominent expression levels of Gadd45a protein in animal tumors. Thus, we confirm that overexpression of Gadd45a in combination with ionizing radiation has therapeutic implications by preventing recurrence of MMP-9-mediated cancer cell invasion and effectively containing cells in a static phase by maintaining CCA/CCI. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 576. doi:10.1158/1538-7445.AM2011-576
    Materialart: Online-Ressource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2011-576
    RVK:
    XA 36000
    RVK:
    XA 10000
    Sprache: Englisch
    Verlag: American Association for Cancer Research (AACR)
    Publikationsdatum: 2011
    ZDB Id: 2036785-5
    ZDB Id: 1432-1
    ZDB Id: 410466-3
    Standort Signatur Einschränkungen Verfügbarkeit
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