Natalya V Guseva

Summary

Affiliation: University of Iowa
Country: USA

Publications

  1. ncbi P53 and the proteasome regulate androgen receptor activity
    Natalya V Guseva
    Department of Pathology, University of Iowa, Iowa City, Iowa, USA
    Cancer Biol Ther 13:553-8. 2012
  2. ncbi Inhibition of p53 expression modifies the specificity of chromatin binding by the androgen receptor
    Natalya V Guseva
    Department of Pathology, University of Iowa Hospitals and Clinics, Iowa City, Iowa, USA
    Oncotarget 3:183-94. 2012
  3. ncbi TOFA (5-tetradecyl-oxy-2-furoic acid) reduces fatty acid synthesis, inhibits expression of AR, neuropilin-1 and Mcl-1 and kills prostate cancer cells independent of p53 status
    Natalya V Guseva
    University of Iowa, Iowa City, USA
    Cancer Biol Ther 12:80-5. 2011
  4. ncbi KN-93 inhibits androgen receptor activity and induces cell death irrespective of p53 and Akt status in prostate cancer
    Oskar W Rokhlin
    Department of Pathology, The University of Iowa, Iowa City, IA, USA
    Cancer Biol Ther 9:224-35. 2010
  5. ncbi Mechanisms of cell death induced by histone deacetylase inhibitors in androgen receptor-positive prostate cancer cells
    Oskar W Rokhlin
    Department of Pathology, University of Iowa, Iowa City, IA 52242, USA
    Mol Cancer Res 4:113-23. 2006
  6. ncbi TSA-induced cell death in prostate cancer cell lines is caspase-2 dependent and involves the PIDDosome
    Agshin F Taghiyev
    Department of Pathology, The University of Iowa, Iowa City, Iowa 52242-1087, USA
    Cancer Biol Ther 5:1199-205. 2006
  7. ncbi Overexpression of BAD potentiates sensitivity to tumor necrosis factor-related apoptosis-inducing ligand treatment in the prostatic carcinoma cell line LNCaP
    Agshin F Taghiyev
    Department of Pathology, The University of Iowa, 200 Hawkins Drive, Iowa City, IA 52242 1087, USA
    Mol Cancer Res 1:500-7. 2003
  8. ncbi Multiple effects of N-alpha-tosyl-L-phenylalanyl chloromethyl ketone (TPCK) on apoptotic pathways in human prostatic carcinoma cell lines
    Oskar W Rokhlin
    Department of Pathology, The University of Iowa, Iowa City, Iowa 52242, USA
    Cancer Biol Ther 3:761-8. 2004
  9. ncbi Trichostatin A (TSA) sensitizes the human prostatic cancer cell line DU145 to death receptor ligands treatment
    Agshin F Taghiyev
    Department of Pathology, The University of Iowa, Iowa City, Iowa, USA
    Cancer Biol Ther 4:382-90. 2005
  10. ncbi Tumor necrosis factor-related apoptosis-inducing ligand-mediated activation of mitochondria-associated nuclear factor-kappaB in prostatic carcinoma cell lines
    Natalya V Guseva
    Department of Pathology, University of Iowa, 200 Hawkins Drive, Iowa City, IA 52242 1087, USA
    Mol Cancer Res 2:574-84. 2004

Collaborators

Detail Information

Publications17

  1. ncbi P53 and the proteasome regulate androgen receptor activity
    Natalya V Guseva
    Department of Pathology, University of Iowa, Iowa City, Iowa, USA
    Cancer Biol Ther 13:553-8. 2012
    ..Therefore, the role of p53 during treatment with proteasome inhibitors in different tumors should be further investigated...
  2. ncbi Inhibition of p53 expression modifies the specificity of chromatin binding by the androgen receptor
    Natalya V Guseva
    Department of Pathology, University of Iowa Hospitals and Clinics, Iowa City, Iowa, USA
    Oncotarget 3:183-94. 2012
    ..Overall, our results point to p53 playing an important role in regulating AR activity across the genome...
  3. ncbi TOFA (5-tetradecyl-oxy-2-furoic acid) reduces fatty acid synthesis, inhibits expression of AR, neuropilin-1 and Mcl-1 and kills prostate cancer cells independent of p53 status
    Natalya V Guseva
    University of Iowa, Iowa City, USA
    Cancer Biol Ther 12:80-5. 2011
    ..Here, we show for the first time that NRP1 expression is under AR control. Taken together, our data suggest that TOFA is a potent cell death inducing agent in prostate cancer cells...
  4. ncbi KN-93 inhibits androgen receptor activity and induces cell death irrespective of p53 and Akt status in prostate cancer
    Oskar W Rokhlin
    Department of Pathology, The University of Iowa, Iowa City, IA, USA
    Cancer Biol Ther 9:224-35. 2010
    ..These data suggest that KN-93 could be used for novel therapeutic approaches when hormonal therapy has failed...
  5. ncbi Mechanisms of cell death induced by histone deacetylase inhibitors in androgen receptor-positive prostate cancer cells
    Oskar W Rokhlin
    Department of Pathology, University of Iowa, Iowa City, IA 52242, USA
    Mol Cancer Res 4:113-23. 2006
    ..The synergistic effect of simultaneous treatment with trichostatin A and doxorubicin is mediated via inhibition of AR expression, induction of protease activity, increased expression of p53, and proteolysis of p21...
  6. ncbi TSA-induced cell death in prostate cancer cell lines is caspase-2 dependent and involves the PIDDosome
    Agshin F Taghiyev
    Department of Pathology, The University of Iowa, Iowa City, Iowa 52242-1087, USA
    Cancer Biol Ther 5:1199-205. 2006
    ..Together, these data indicate that caspase-2 initiates caspase cascade after TSA treatment and involves the formation of the PIDDosome...
  7. ncbi Overexpression of BAD potentiates sensitivity to tumor necrosis factor-related apoptosis-inducing ligand treatment in the prostatic carcinoma cell line LNCaP
    Agshin F Taghiyev
    Department of Pathology, The University of Iowa, 200 Hawkins Drive, Iowa City, IA 52242 1087, USA
    Mol Cancer Res 1:500-7. 2003
    ..Lastly, recombinant BAD cleaved by caspase-3 is a more potent inducer of cytochrome c and Smac/DIABLO release than BAD WT. In summary, BAD-mediated sensitivity of LNCaP to TRAIL depends on the phosphorylation status of BAD WT and tBAD...
  8. ncbi Multiple effects of N-alpha-tosyl-L-phenylalanyl chloromethyl ketone (TPCK) on apoptotic pathways in human prostatic carcinoma cell lines
    Oskar W Rokhlin
    Department of Pathology, The University of Iowa, Iowa City, Iowa 52242, USA
    Cancer Biol Ther 3:761-8. 2004
    ..Together, these features suggest that TPCK could be used as a therapeutic agent for treatment of those tumor cells that are resistant to ligand-induced treatment because of aberrant signaling pathways downstream of the DISC...
  9. ncbi Trichostatin A (TSA) sensitizes the human prostatic cancer cell line DU145 to death receptor ligands treatment
    Agshin F Taghiyev
    Department of Pathology, The University of Iowa, Iowa City, Iowa, USA
    Cancer Biol Ther 4:382-90. 2005
    ..The combination of TSA and TNF-family ligands could potentially be the basis for the treatment of prostate cancer...
  10. ncbi Tumor necrosis factor-related apoptosis-inducing ligand-mediated activation of mitochondria-associated nuclear factor-kappaB in prostatic carcinoma cell lines
    Natalya V Guseva
    Department of Pathology, University of Iowa, 200 Hawkins Drive, Iowa City, IA 52242 1087, USA
    Mol Cancer Res 2:574-84. 2004
    ..In summary, NF-kappaB is found in mitochondria of prostatic carcinoma cells, where it is thought to regulate mitochondria genome encoded mRNA levels in response to TRAIL treatment...
  11. ncbi Androgen regulates apoptosis induced by TNFR family ligands via multiple signaling pathways in LNCaP
    Oskar W Rokhlin
    Department of Pathology, University of Iowa, Iowa City, 1163 ML, IA, USA
    Oncogene 24:6773-84. 2005
    ..Our study suggests that androgen-dependent outcome of apoptotic treatment can occur, at least in part, via the caspase-2, Akt and p53-mediated pathways...
  12. ncbi Death receptor-induced cell death in prostate cancer
    Natalya V Guseva
    Department of Pathology, University of Iowa, Iowa City, Iowa 52242-1087, USA
    J Cell Biochem 91:70-99. 2004
    ..In this review we have focused on what is known about apoptosis in prostate cancer and, more specifically, the receptor/ligand-mediated pathways of apoptosis as potential therapeutic targets...
  13. ncbi Unique resistance of breast carcinoma cell line T47D to TRAIL but not anti-Fas is linked to p43cFLIP(L)
    Natalya V Guseva
    Department of Pathology, The University of Iowa, 200 Hawkins Drive, C670, Iowa City, IA 52242 1087, USA
    Breast Cancer Res Treat 107:349-57. 2008
    ..We propose that in T47D p43 cFLIP(L) in the Fas-DISC may promote caspase-8 activation. The mechanism by which different amounts of p43cFLIP(L) regulates caspase-8 activation remains to be investigated...
  14. ncbi Bisindolylmaleimide IX facilitates tumor necrosis factor receptor family-mediated cell death and acts as an inhibitor of transcription
    Oskar W Rokhlin
    Department of Pathology, The University of Iowa, Iowa City, Iowa 52242, USA
    J Biol Chem 277:33213-9. 2002
    ..In summary, these results suggest that Bis IX potentiates TNF receptor family-mediated cell death in part as an inhibitor of transcription...
  15. ncbi Glycosylation contributes to variability in expression of murine cytomegalovirus m157 and enhances stability of interaction with the NK-cell receptor Ly49H
    Natalya V Guseva
    Department of Pathology, Roy J and Lucille A Carver College of Medicine, Iowa City, IA 52242, USA
    Eur J Immunol 40:2618-31. 2010
    ..Thus, glycosylation on m157 enhances expression and binding to Ly49H, factors that may impact the interaction between NK cells and MCMV in vivo where receptor-ligand interactions are more limiting...
  16. ncbi Contribution of death receptor and mitochondrial pathways to Fas-mediated apoptosis in the prostatic carcinoma cell line PC3
    Natalya V Guseva
    Department of Pathology, The University of Iowa, Iowa City, Iowa 52242-1087, USA
    Prostate 51:231-40. 2002
    ..In addition, caspase-3 activation after Fas-receptor ligation involves two steps and is dependent on mitochondrial activation...
  17. ncbi Characterization of murine cytomegalovirus m157 from infected cells and identification of critical residues mediating recognition by the NK cell receptor Ly49H
    Aja H Davis
    Department of Pathology, Roy J and Lucille A Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA
    J Immunol 181:265-75. 2008
    ..These findings support an emerging model for a novel interaction between this important NK cell receptor and its viral ligand...