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  1. AU=Nagaprashantha Lokesh Dalasanur AU=Nagaprashantha Lokesh Dalasanur
  2. AU="Coquerel, David"
  3. AU="Mofenson, Lynne"
  4. AU="Ochir, Chimedsuren"
  5. AU="Nimmagadda, Vamshi K C"
  6. AU="Apablaza, Natalia"
  7. AU="Feyaerts, Dorien"
  8. AU="Hasegawa, Yoshimi"
  9. AU="Obata, Soichiro"
  10. AU=Tyrrell P
  11. AU=Fessler M Margaret
  12. AU=Ashrafzadeh Sepideh AU=Ashrafzadeh Sepideh
  13. AU="Kellie Leigh"
  14. AU="Nogueira, Fábio"
  15. AU="Davidson, Rose K."
  16. AU="Belkin, Igor M."
  17. AU="Cui, Rongxin"
  18. AU="Lassmann-Vague, V"
  19. AU="Schmit, Megan"
  20. AU="Donato, Federica"
  21. AU="Bommineni, Yugendar R"
  22. AU="Qi, Zhaoyu"
  23. AU=Campos Daniel Melo De Oliveira AU=Campos Daniel Melo De Oliveira
  24. AU="Ashish, Kumar"
  25. AU="Franziska Press"
  26. AU=Eickmann Markus
  27. AU=Shukla Prashant
  28. AU="Fernández-Fernández, Luis"
  29. AU="Hall, Dylan"
  30. AU="Peiró, Juanjo"
  31. AU="Qi, Hong"
  32. AU="Man, William D-C"
  33. AU="Ko, Hyunsuk"
  34. AU="Lucas, Jonathan"
  35. AU="Palomar-Bonet, Miriam"
  36. AU="Rho, Seongheon"
  37. AU="Proux-Gillardeaux, Veronique"
  38. AU="Menon, Kartikeya M"
  39. AU="Pantell, Matthew" AU="Pantell, Matthew"
  40. AU="Maria Papadopoulou"
  41. AU="Wu, Jianrong"
  42. AU="Rodrigues, Daniel Sobreira"
  43. AU="Angello R. Retamal-Díaz"
  44. AU="Nicole C. Deziel"
  45. AU="Shajrawi, Abedalmajeed Methqal"
  46. AU=Aydin Seckin AU=Aydin Seckin
  47. AU="Narwal, Vikrant"
  48. AU="Minamoto, Toshinari"

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  1. Artikel ; Online: Correction: 2'-Hydroxyflavanone effectively targets RLIP76-mediated drug transport and regulates critical signaling networks in breast cancer.

    Nagaprashantha, Lokesh Dalasanur / Singhal, Jyotsana / Li, Hongzhi / Warden, Charles / Liu, Xueli / Horne, David / Awasthi, Sanjay / Salgia, Ravi / Singhal, Sharad S

    Oncotarget

    2022  Band 13, Seite(n) 331

    Abstract: This corrects the article DOI: 10.18632/oncotarget.24720.]. ...

    Abstract [This corrects the article DOI: 10.18632/oncotarget.24720.].
    Sprache Englisch
    Erscheinungsdatum 2022-02-11
    Erscheinungsland United States
    Dokumenttyp Published Erratum
    ZDB-ID 2560162-3
    ISSN 1949-2553 ; 1949-2553
    ISSN (online) 1949-2553
    ISSN 1949-2553
    DOI 10.18632/oncotarget.28199
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: 2'-Hydroxyflavanone effectively targets RLIP76-mediated drug transport and regulates critical signaling networks in breast cancer.

    Nagaprashantha, Lokesh Dalasanur / Singhal, Jyotsana / Li, Hongzhi / Warden, Charles / Liu, Xueli / Horne, David / Awasthi, Sanjay / Salgia, Ravi / Singhal, Sharad S

    Oncotarget

    2018  Band 9, Heft 26, Seite(n) 18053–18068

    Abstract: Breast cancer (BC) is the most common cancer in women. Estrogen, epidermal growth factor receptor 2 (ERBB2, HER2), and oxidative stress represent critical mechanistic nodes associated with BC. RLIP76 is a major mercapturic acid pathway transporter whose ... ...

    Abstract Breast cancer (BC) is the most common cancer in women. Estrogen, epidermal growth factor receptor 2 (ERBB2, HER2), and oxidative stress represent critical mechanistic nodes associated with BC. RLIP76 is a major mercapturic acid pathway transporter whose expression is increased in BC. In the quest of a novel molecule with chemopreventive and chemotherapeutic potential, we evaluated the effects of 2'-Hydroxyflavanone (2HF) in BC. 2HF enhanced the inhibitory effects of RLIP76 depletion and also inhibited RLIP76-mediated doxorubicin transport in BC cells. RNA-sequencing revealed that 2HF induces strong reversal of the gene expression pattern in ER
    Sprache Englisch
    Erscheinungsdatum 2018-04-06
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 2560162-3
    ISSN 1949-2553 ; 1949-2553
    ISSN (online) 1949-2553
    ISSN 1949-2553
    DOI 10.18632/oncotarget.24720
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Oxidative stress and dietary phytochemicals: Role in cancer chemoprevention and treatment.

    Chikara, Shireen / Nagaprashantha, Lokesh Dalasanur / Singhal, Jyotsana / Horne, David / Awasthi, Sanjay / Singhal, Sharad S

    Cancer letters

    2017  Band 413, Seite(n) 122–134

    Abstract: Several epidemiological observations have shown an inverse relation between consumption of plant-based foods, rich in phytochemicals, and incidence of cancer. Phytochemicals, secondary plant metabolites, via their antioxidant property play a key role in ... ...

    Abstract Several epidemiological observations have shown an inverse relation between consumption of plant-based foods, rich in phytochemicals, and incidence of cancer. Phytochemicals, secondary plant metabolites, via their antioxidant property play a key role in cancer chemoprevention by suppressing oxidative stress-induced DNA damage. In addition, they modulate several oxidative stress-mediated signaling pathways through their anti-oxidant effects, and ultimately protect cells from undergoing molecular changes that trigger carcinogenesis. In several instances, however, the pro-oxidant property of these phytochemicals has been observed with respect to cancer treatment. Further, in vitro and in vivo studies show that several phytochemicals potentiate the efficacy of chemotherapeutic agents by exacerbating oxidative stress in cancer cells. Therefore, we reviewed multiple studies investigating the role of dietary phytochemicals such as, curcumin (turmeric), epigallocatechin gallate (EGCG; green tea), resveratrol (grapes), phenethyl isothiocyanate (PEITC), sulforaphane (cruciferous vegetables), hesperidin, quercetin and 2'-hydroxyflavanone (2HF; citrus fruits) in regulating oxidative stress and associated signaling pathways in the context of cancer chemoprevention and treatment.
    Mesh-Begriff(e) Animals ; Anticarcinogenic Agents/therapeutic use ; Antineoplastic Agents, Phytogenic/therapeutic use ; Antioxidants/therapeutic use ; Diet ; Drug Resistance, Neoplasm ; Humans ; Neoplasms/metabolism ; Neoplasms/pathology ; Neoplasms/prevention & control ; Oxidative Stress/drug effects ; Phytochemicals/therapeutic use ; Signal Transduction/drug effects
    Chemische Substanzen Anticarcinogenic Agents ; Antineoplastic Agents, Phytogenic ; Antioxidants ; Phytochemicals
    Sprache Englisch
    Erscheinungsdatum 2017-11-04
    Erscheinungsland Ireland
    Dokumenttyp Journal Article ; Review ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't
    ZDB-ID 195674-7
    ISSN 1872-7980 ; 0304-3835
    ISSN (online) 1872-7980
    ISSN 0304-3835
    DOI 10.1016/j.canlet.2017.11.002
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: Translational opportunities for broad-spectrum natural phytochemicals and targeted agent combinations in breast cancer.

    Dalasanur Nagaprashantha, Lokesh / Adhikari, Ramesh / Singhal, Jyotsana / Chikara, Shireen / Awasthi, Sanjay / Horne, David / Singhal, Sharad S

    International journal of cancer

    2017  Band 142, Heft 4, Seite(n) 658–670

    Abstract: Breast cancer (BC) prevention and therapy in the context of life-style risk factors and biological drivers is a major focus of developmental therapeutics in oncology. Obesity, alcohol, chronic estrogen signaling and smoking have distinct BC precipitating ...

    Abstract Breast cancer (BC) prevention and therapy in the context of life-style risk factors and biological drivers is a major focus of developmental therapeutics in oncology. Obesity, alcohol, chronic estrogen signaling and smoking have distinct BC precipitating and facilitating effects that may act alone or in combination. A spectrum of signaling events including enhanced oxidative stress and changes in estrogen-receptor (ER)-dependent and -independent signaling drive the progression of BC. Breast tumors modulate ERα/ERβ ratio, upregulate proliferative pathways driven by ERα and HER2 with a parallel loss and/or downregulation of tumor suppressors such as TP53 and PTEN which together impact the efficacy of therapeutic strategies and frequently lead to emergence of drug resistance. Natural phytochemicals modulate oxidative stress, leptin, integrin, HER2, MAPK, ERK, Wnt/β-catenin and NFκB signaling along with regulating ERα and ERβ, thereby presenting unique opportunities for both primary and combinatorial interventions in BC. In this regard, this article focuses on critical analyses of the evidence from multiple studies on the efficacy of natural phytochemicals in BC. In addition, areas in which the combinations of such effective natural phytochemicals with approved and/or developing anticancer agents can be translationally beneficial are discussed to derive evidence-based inference for addressing challenges in BC control and therapy.
    Mesh-Begriff(e) Biomarkers, Tumor/antagonists & inhibitors ; Breast Neoplasms/metabolism ; Breast Neoplasms/prevention & control ; Drug Therapy, Combination ; Female ; Humans ; Molecular Targeted Therapy ; Phytochemicals/therapeutic use ; Translational Medical Research
    Chemische Substanzen Biomarkers, Tumor ; Phytochemicals
    Sprache Englisch
    Erscheinungsdatum 2017-11-28
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Review
    ZDB-ID 218257-9
    ISSN 1097-0215 ; 0020-7136
    ISSN (online) 1097-0215
    ISSN 0020-7136
    DOI 10.1002/ijc.31085
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.MO 576: Hefte anzeigen

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  5. Artikel ; Online: RLIP76 regulates PI3K/Akt signaling and chemo-radiotherapy resistance in pancreatic cancer.

    Kathryn Leake / Jyotsana Singhal / Lokesh Dalasanur Nagaprashantha / Sanjay Awasthi / Sharad S Singhal

    PLoS ONE, Vol 7, Iss 4, p e

    2012  Band 34582

    Abstract: Pancreatic cancer is an aggressive malignancy with characteristic metastatic course of disease and resistance to conventional chemo-radiotherapy. RLIP76 is a multi-functional cell membrane protein that functions as a major mercapturic acid pathway ... ...

    Abstract Pancreatic cancer is an aggressive malignancy with characteristic metastatic course of disease and resistance to conventional chemo-radiotherapy. RLIP76 is a multi-functional cell membrane protein that functions as a major mercapturic acid pathway transporter as well as key regulator of receptor-ligand complexes. In this regard, we investigated the significance of targeting RLIP76 on PI3K/Akt pathway and mechanisms regulating response to chemo-radiotherapy.Cell survival was assessed by MTT and colony forming assays. Cellular levels of proteins and phosphorylation was determined by Western blot analyses. The impact on apoptosis was determined by TUNEL assay. The anti-cancer effects of RLIP76 targeted interventions in vivo were determined using mice xenograft model of the pancreatic cancer. The regulation of doxorubicin transport and radiation sensitivity were determined by transport studies and colony forming assays, respectively.Our current studies reveal an encompassing model for the role of RLIP76 in regulating the levels of fundamental proteins like PI3K, Akt, E-cadherin, CDK4, Bcl2 and PCNA which are of specific importance in the signal transduction from critical upstream signaling cascades that determine the proliferation, apoptosis and differentiation of pancreatic cancer cells. RLIP76 depletion also caused marked and sustained regression of established human BxPC-3 pancreatic cancer tumors in nude mouse xenograft model. RLIP76 turned out to be a major regulator of drug transport along with contributing to the radiation resistance in pancreatic cancer.RLIP76 represents a mechanistically significant target for developing effective interventions in aggressive and refractory pancreatic cancers.
    Schlagwörter Medicine ; R ; Science ; Q
    Thema/Rubrik (Code) 610 ; 500
    Sprache Englisch
    Erscheinungsdatum 2012-01-01T00:00:00Z
    Verlag Public Library of Science (PLoS)
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  6. Artikel ; Online: RLIP76 regulates PI3K/Akt signaling and chemo-radiotherapy resistance in pancreatic cancer.

    Leake, Kathryn / Singhal, Jyotsana / Nagaprashantha, Lokesh Dalasanur / Awasthi, Sanjay / Singhal, Sharad S

    PloS one

    2012  Band 7, Heft 4, Seite(n) e34582

    Abstract: Purpose: Pancreatic cancer is an aggressive malignancy with characteristic metastatic course of disease and resistance to conventional chemo-radiotherapy. RLIP76 is a multi-functional cell membrane protein that functions as a major mercapturic acid ... ...

    Abstract Purpose: Pancreatic cancer is an aggressive malignancy with characteristic metastatic course of disease and resistance to conventional chemo-radiotherapy. RLIP76 is a multi-functional cell membrane protein that functions as a major mercapturic acid pathway transporter as well as key regulator of receptor-ligand complexes. In this regard, we investigated the significance of targeting RLIP76 on PI3K/Akt pathway and mechanisms regulating response to chemo-radiotherapy.
    Research design and methods: Cell survival was assessed by MTT and colony forming assays. Cellular levels of proteins and phosphorylation was determined by Western blot analyses. The impact on apoptosis was determined by TUNEL assay. The anti-cancer effects of RLIP76 targeted interventions in vivo were determined using mice xenograft model of the pancreatic cancer. The regulation of doxorubicin transport and radiation sensitivity were determined by transport studies and colony forming assays, respectively.
    Results: Our current studies reveal an encompassing model for the role of RLIP76 in regulating the levels of fundamental proteins like PI3K, Akt, E-cadherin, CDK4, Bcl2 and PCNA which are of specific importance in the signal transduction from critical upstream signaling cascades that determine the proliferation, apoptosis and differentiation of pancreatic cancer cells. RLIP76 depletion also caused marked and sustained regression of established human BxPC-3 pancreatic cancer tumors in nude mouse xenograft model. RLIP76 turned out to be a major regulator of drug transport along with contributing to the radiation resistance in pancreatic cancer.
    Conclusions/significance: RLIP76 represents a mechanistically significant target for developing effective interventions in aggressive and refractory pancreatic cancers.
    Mesh-Begriff(e) Animals ; Apoptosis/drug effects ; Apoptosis/genetics ; Apoptosis/radiation effects ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cell Proliferation/radiation effects ; Cell Survival/drug effects ; Cell Survival/genetics ; Cell Survival/radiation effects ; Cell Transformation, Neoplastic ; Chemoradiotherapy ; Doxorubicin/metabolism ; Doxorubicin/pharmacology ; GTPase-Activating Proteins/deficiency ; GTPase-Activating Proteins/genetics ; GTPase-Activating Proteins/metabolism ; Gene Expression Regulation, Neoplastic/drug effects ; Gene Expression Regulation, Neoplastic/genetics ; Gene Expression Regulation, Neoplastic/radiation effects ; Gene Knockdown Techniques ; Humans ; Mice ; Pancreatic Neoplasms/metabolism ; Pancreatic Neoplasms/pathology ; Pancreatic Neoplasms/therapy ; Phosphatidylinositol 3-Kinases/metabolism ; Protein Transport/drug effects ; Protein Transport/genetics ; Protein Transport/radiation effects ; Proto-Oncogene Proteins c-akt/metabolism ; RNA, Small Interfering/genetics ; Radiation Tolerance/genetics ; Signal Transduction/drug effects ; Signal Transduction/radiation effects ; Treatment Failure
    Chemische Substanzen GTPase-Activating Proteins ; RNA, Small Interfering ; Ralbp1 protein, mouse ; Doxorubicin (80168379AG) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
    Sprache Englisch
    Erscheinungsdatum 2012-04-03
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0034582
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel ; Online: Targeting p53-null neuroblastomas through RLIP76.

    Singhal, Jyotsana / Yadav, Sushma / Nagaprashantha, Lokesh Dalasanur / Vatsyayan, Rit / Singhal, Sharad S / Awasthi, Sanjay

    Cancer prevention research (Philadelphia, Pa.)

    2011  Band 4, Heft 6, Seite(n) 879–889

    Abstract: The search for p53-independent mechanism of cancer cell killing is highly relevant to pediatric neuroblastomas, where successful therapy is limited by its transformation into p53-mutant and a highly drug-resistant neoplasm. Our studies on the drug- ... ...

    Abstract The search for p53-independent mechanism of cancer cell killing is highly relevant to pediatric neuroblastomas, where successful therapy is limited by its transformation into p53-mutant and a highly drug-resistant neoplasm. Our studies on the drug-resistant p53-mutant as compared with drug-resistant p53 wild-type neuroblastoma revealed a novel mechanism for resistance to apoptosis: a direct role of p53 in regulating the cellular concentration of proapoptotic alkenals by functioning as a specific and saturable allosteric inhibitor of the alkenal-glutathione conjugate transporter, RLIP76. The RLIP76-p53 complex was showed by both immunoprecipitation analyses of purified proteins and immunofluorescence analysis. Drug transport studies revealed that p53 inhibited both basal and PKCα-stimulated transport of glutathione conjugates of 4HNE (GSHNE) and doxorubicin. Drug resistance was significantly greater for p53-mutant as compared with p53 wild-type neuroblastoma cell lines, but both were susceptible to depletion of RLIP76 by antisense alone. In addition, inhibition of RLIP76 significantly enhanced the cytotoxicity of cisplatin. Taken together, these studies provide powerful evidence for a novel mechanism for drug and apoptosis resistance in p53-mutant neuroblastoma, based on a model of regulation of p53-induced apoptosis by RLIP76, where p53 is a saturable and specific allosteric inhibitor of RLIP76, and p53 loss results in overexpression of RLIP76; thus, in the absence of p53, the drug and glutathione-conjugate transport activities of RLIP76 are enhanced. Most importantly, our findings strongly indicate RLIP76 as a novel target for therapy of drug-resistant and p53-mutant neuroblastoma.
    Mesh-Begriff(e) ATP-Binding Cassette Transporters/antagonists & inhibitors ; ATP-Binding Cassette Transporters/genetics ; ATP-Binding Cassette Transporters/metabolism ; Animals ; Antineoplastic Combined Chemotherapy Protocols/pharmacology ; Blotting, Western ; Child ; Cisplatin/administration & dosage ; Cross-Linking Reagents/pharmacology ; Doxorubicin/administration & dosage ; Drug Resistance, Multiple ; Drug Resistance, Neoplasm/genetics ; GTPase-Activating Proteins/antagonists & inhibitors ; GTPase-Activating Proteins/genetics ; GTPase-Activating Proteins/metabolism ; Glutathione/metabolism ; Humans ; Immunoenzyme Techniques ; Immunoprecipitation ; Male ; Mice ; Mice, Nude ; Neuroblastoma/genetics ; Neuroblastoma/metabolism ; Neuroblastoma/prevention & control ; Oligonucleotides, Antisense/pharmacology ; Tumor Cells, Cultured ; Tumor Suppressor Protein p53/physiology
    Chemische Substanzen ATP-Binding Cassette Transporters ; Cross-Linking Reagents ; GTPase-Activating Proteins ; Oligonucleotides, Antisense ; RALBP1 protein, human ; TP53 protein, human ; Tumor Suppressor Protein p53 ; Doxorubicin (80168379AG) ; Glutathione (GAN16C9B8O) ; Cisplatin (Q20Q21Q62J)
    Sprache Englisch
    Erscheinungsdatum 2011-03-16
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 2434717-6
    ISSN 1940-6215 ; 1940-6207
    ISSN (online) 1940-6215
    ISSN 1940-6207
    DOI 10.1158/1940-6207.CAPR-11-0025
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  8. Artikel ; Online: Proteomic analysis of signaling network regulation in renal cell carcinomas with differential hypoxia-inducible factor-2α expression.

    Lokesh Dalasanur Nagaprashantha / Tatjana Talamantes / Jyotsana Singhal / Jia Guo / Rit Vatsyayan / Navin Rauniyar / Sanjay Awasthi / Sharad S Singhal / Laszlo Prokai

    PLoS ONE, Vol 8, Iss 8, p e

    2013  Band 71654

    Abstract: The loss of von Hippel-Lindau (VHL) protein function leads to highly vascular renal tumors characterized by an aggressive course of disease and refractoriness to chemotherapy and radiotherapy. Loss of VHL in renal tumors also differs from tumors of other ...

    Abstract The loss of von Hippel-Lindau (VHL) protein function leads to highly vascular renal tumors characterized by an aggressive course of disease and refractoriness to chemotherapy and radiotherapy. Loss of VHL in renal tumors also differs from tumors of other organs in that the oncogenic cascade is mediated by an increase in the levels of hypoxia-inducible factor-2α (HIF2α) instead of hypoxia-inducible factor-1α (HIF1α).We used renal carcinoma cell lines that recapitulate the differences between mutant VHL and wild-type VHL genotypes. Utilizing a method relying on extracted peptide intensities as a label-free approach for quantitation by liquid chromatography-mass spectrometry, our proteomics study revealed regulation of key proteins important for cancer cell survival, proliferation and stress-resistance, and implicated differential regulation of signaling networks in VHL-mutant renal cell carcinoma. We also observed upregulation of cellular energy pathway enzymes and the stress-responsive mitochondrial 60-kDa heat shock protein. Finding reliance on glutaminolysis in VHL-mutant renal cell carcinoma was of particular significance, given the generally predominant dependence of tumors on glycolysis. The data have been deposited to the ProteomeXchange with identifier PXD000335.Pathway analyses provided corroborative evidence for differential regulation of molecular and cellular functions influencing cancer energetics, metabolism and cell proliferation in renal cell carcinoma with distinct VHL genotype. Collectively, the differentially regulated proteome characterized by this study can potentially guide translational research specifically aimed at effective clinical interventions for advanced VHL-mutant, HIF2α-over-expressing tumors.
    Schlagwörter Medicine ; R ; Science ; Q
    Thema/Rubrik (Code) 616
    Sprache Englisch
    Erscheinungsdatum 2013-01-01T00:00:00Z
    Verlag Public Library of Science (PLoS)
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  9. Artikel ; Online: Didymin induces apoptosis by inhibiting N-Myc and upregulating RKIP in neuroblastoma.

    Singhal, Jyotsana / Nagaprashantha, Lokesh Dalasanur / Vatsyayan, Rit / Ashutosh / Awasthi, Sanjay / Singhal, Sharad S

    Cancer prevention research (Philadelphia, Pa.)

    2011  Band 5, Heft 3, Seite(n) 473–483

    Abstract: Neuroblastomas arise from the neural crest cells and represent the most common solid tumors outside the nervous system in children. The amplification of N-Myc plays a primary role in the pathogenesis of neuroblastomas, whereas acquired mutations of p53 ... ...

    Abstract Neuroblastomas arise from the neural crest cells and represent the most common solid tumors outside the nervous system in children. The amplification of N-Myc plays a primary role in the pathogenesis of neuroblastomas, whereas acquired mutations of p53 lead to refractory and relapsed cases of neuroblastomas. In this regard, dietary compounds which can target N-Myc and exert anticancer effects independent of p53 status acquire significance in the management of neuroblastomas. Hence, we investigated the anticancer properties of the flavonoid didymin in neuroblastomas. Didymin effectively inhibited proliferation and induced apoptosis irrespective of p53 status in neuroblastomas. Didymin downregulated phosphoinositide 3-kinase, pAkt, Akt, vimentin, and upregulated RKIP levels. Didymin induced G(2)/M arrest along with decreasing the levels of cyclin D1, CDK4, and cyclin B1. Importantly, didymin inhibited N-Myc as confirmed at protein, mRNA, and transcriptional level by promoter-reporter assays. High-performance liquid chromatography analysis of didymin-treated (2 mg/kg b.w.) mice serum revealed effective oral absorption with free didymin concentration of 2.1 μmol/L. Further in vivo mice xenograft studies revealed that didymin-treated (2 mg/kg b.w.) animals had significant reductions in tumors size compared with controls. Didymin strongly inhibited the proliferation (Ki67) and angiogenesis (CD31) markers, as well as N-Myc expression, as revealed by the histopathologic examination of paraffin-embedded section of resected tumors. Collectively, our in vitro and in vivo studies elucidated the anticancer properties and mechanisms of action of a novel, orally active, and palatable flavonoid didymin, which makes it a potential new approach for neuroblastoma therapy (NANT) to target pediatric neuroblastomas.
    Mesh-Begriff(e) Animals ; Apoptosis/drug effects ; Blotting, Western ; Cell Cycle/drug effects ; Cell Movement/drug effects ; Cell Proliferation/drug effects ; Flavonoids/pharmacology ; Flow Cytometry ; Glycosides/pharmacology ; Humans ; Immunoenzyme Techniques ; Mice ; Mice, Nude ; Neuroblastoma/drug therapy ; Neuroblastoma/metabolism ; Neuroblastoma/pathology ; Phosphatidylethanolamine Binding Protein/antagonists & inhibitors ; Phosphatidylethanolamine Binding Protein/genetics ; Phosphatidylethanolamine Binding Protein/metabolism ; Proto-Oncogene Proteins c-myc/antagonists & inhibitors ; Proto-Oncogene Proteins c-myc/genetics ; Proto-Oncogene Proteins c-myc/metabolism ; RNA, Messenger/genetics ; RNA, Small Interfering/genetics ; Real-Time Polymerase Chain Reaction ; Tumor Cells, Cultured ; Up-Regulation
    Chemische Substanzen Flavonoids ; Glycosides ; PEBP1 protein, human ; Phosphatidylethanolamine Binding Protein ; Proto-Oncogene Proteins c-myc ; RNA, Messenger ; RNA, Small Interfering ; didymin
    Sprache Englisch
    Erscheinungsdatum 2011-12-15
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2434717-6
    ISSN 1940-6215 ; 1940-6207
    ISSN (online) 1940-6215
    ISSN 1940-6207
    DOI 10.1158/1940-6207.CAPR-11-0318
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  10. Artikel ; Online: Nutlin-3 enhances sorafenib efficacy in renal cell carcinoma.

    Vatsyayan, Rit / Singhal, Jyotsana / Nagaprashantha, Lokesh Dalasanur / Awasthi, Sanjay / Singhal, Sharad S

    Molecular carcinogenesis

    2011  Band 52, Heft 1, Seite(n) 39–48

    Abstract: The renal cell carcinoma (RCC) is one of the top 10 cancers in USA. The renal tumors are highly angiogenic and are resistant to conventional interventions, particularly radiotherapy. The advent of multi-specific tyrosine kinase inhibitor sorafenib has ... ...

    Abstract The renal cell carcinoma (RCC) is one of the top 10 cancers in USA. The renal tumors are highly angiogenic and are resistant to conventional interventions, particularly radiotherapy. The advent of multi-specific tyrosine kinase inhibitor sorafenib has improved the progression-free survival in RCC, but overall survival in recurrent and metastatic RCC is still a concern that has lead to characterization of combinatorial regimens. Hence, we studied the effect of combination of nutlin-3, an MDM2 inhibitor, which increases p53 levels, and sorafenib in RCC. Sorafenib along with nutlin-3 synergistically inhibited the cell survival and enhanced caspase-3 cleavage leading to apoptosis in RCC. Nutlin-3 and sorafenib were more effective in reducing the migration of RCC, in combination than as single agents. Sorafenib and nutlin-3 decreased the phosphorylation of vascular endothelial growth factor receptor-2 (VEGFR-2) and ERK along with inducing p53 activity. The sorafenib and nutlin-3 co-treatment lead to enhanced levels of p53, p-p53, and increase in the levels of p53 pro-apoptotic effector PUMA, Bax, and decrease in the anti-apoptotic Bcl-2 levels. Importantly, our studies revealed that sorafenib alone can activate p53 in a concentration dependent manner. Thus, co-treatment of nutlin-3 with sorafenib leads to increased half-life of p53, which in turn can be activated by sorafenib, to induce downstream pro-apoptotic and anti-proliferative effects. This is the first report showing the synergistic effect of sorafenib and nutlin-3 while providing a strong clinical-translational rationale for further testing of sorafenib and nutlin-3 combinatorial regimen in human RCC.
    Mesh-Begriff(e) Antineoplastic Agents/pharmacology ; Antineoplastic Combined Chemotherapy Protocols ; Apoptosis/drug effects ; Apoptosis Regulatory Proteins/analysis ; Benzenesulfonates/pharmacology ; Carcinoma, Renal Cell/drug therapy ; Caspase 3/metabolism ; Cell Line, Tumor ; Cell Movement/drug effects ; Humans ; Imidazoles/pharmacology ; Kidney Neoplasms/drug therapy ; MAP Kinase Signaling System/drug effects ; Niacinamide/analogs & derivatives ; Phenylurea Compounds ; Phosphorylation ; Piperazines/pharmacology ; Proto-Oncogene Proteins/analysis ; Proto-Oncogene Proteins c-bcl-2/analysis ; Proto-Oncogene Proteins c-mdm2/antagonists & inhibitors ; Pyridines/pharmacology ; Sorafenib ; Tumor Suppressor Protein p53/analysis ; Vascular Endothelial Growth Factor Receptor-2/metabolism ; bcl-2-Associated X Protein/analysis
    Chemische Substanzen Antineoplastic Agents ; Apoptosis Regulatory Proteins ; BAX protein, human ; BBC3 protein, human ; Benzenesulfonates ; Imidazoles ; Phenylurea Compounds ; Piperazines ; Proto-Oncogene Proteins ; Proto-Oncogene Proteins c-bcl-2 ; Pyridines ; TP53 protein, human ; Tumor Suppressor Protein p53 ; bcl-2-Associated X Protein ; Niacinamide (25X51I8RD4) ; nutlin 3 (53IA0V845C) ; Sorafenib (9ZOQ3TZI87) ; MDM2 protein, human (EC 2.3.2.27) ; Proto-Oncogene Proteins c-mdm2 (EC 2.3.2.27) ; Vascular Endothelial Growth Factor Receptor-2 (EC 2.7.10.1) ; Caspase 3 (EC 3.4.22.-)
    Sprache Englisch
    Erscheinungsdatum 2011-10-17
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1004029-8
    ISSN 1098-2744 ; 0899-1987
    ISSN (online) 1098-2744
    ISSN 0899-1987
    DOI 10.1002/mc.20875
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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