scholarly journals Induction of wild-type p53 activity in human cancer cells by ribozymes that repair mutant p53 transcripts

2000 ◽  
Vol 97 (15) ◽  
pp. 8490-8494 ◽  
Author(s):  
T. Watanabe ◽  
B. A. Sullenger
Keyword(s):  
Cancer Cells ◽  
Human Cancer ◽  
Mutant P53 ◽  
Wild Type ◽  
Human Cancer Cells ◽  
Wild Type P53

scholarly journals Failure of wild-type p53 gene therapy in human cancer cells expressing a mutant p53 protein

Gene Therapy ◽  
1999 ◽  
Vol 6 (1) ◽  
pp. 22-33 ◽  
Author(s):  
A Vinyals ◽  
M A Peinado ◽  
M Gonzalez-Garrigues ◽  
M Monzó ◽  
R D Bonfil ◽  
...  
Keyword(s):  
Gene Therapy ◽  
Cancer Cells ◽  
Human Cancer ◽  
P53 Protein ◽  
P53 Gene ◽  
Mutant P53 ◽  
Wild Type ◽  
Human Cancer Cells ◽  
Wild Type P53

scholarly journals Differential involvement of the CD95 (Fas/APO-1) receptor/ligand system on apoptosis induced by the wild-type p53 gene transfer in human cancer cells

Oncogene ◽  
1999 ◽  
Vol 18 (13) ◽  
pp. 2189-2199 ◽  
Author(s):  
Takuya Fukazawa ◽  
Toshiyoshi Fujiwara ◽  
Yoshinori Morimoto ◽  
Jianghua Shao ◽  
Masahiko Nishizaki ◽  
...  
Keyword(s):  
Gene Transfer ◽  
Cancer Cells ◽  
Human Cancer ◽  
P53 Gene ◽  
Wild Type ◽  
Receptor Ligand ◽  
Human Cancer Cells ◽  
Ligand System ◽  
Differential Involvement ◽  
Wild Type P53

scholarly journals Docosahexaenoic acid induces autophagy through p53/AMPK/mTOR signaling and promotes apoptosis in human cancer cells harboring wild-type p53

Autophagy ◽  
2011 ◽  
Vol 7 (11) ◽  
pp. 1348-1358 ◽  
Author(s):  
Kaipeng Jing ◽  
Kyoung-Sub Song ◽  
Soyeon Shin ◽  
Nayeong Kim ◽  
Soyeon Jeong ◽  
...  
Keyword(s):  
Docosahexaenoic Acid ◽  
Cancer Cells ◽  
Human Cancer ◽  
Mtor Signaling ◽  
Wild Type ◽  
Human Cancer Cells ◽  
Wild Type P53

scholarly journals Telomere erosion triggers growth arrest but not cell death in human cancer cells retaining wild-type p53: implications for antitelomerase therapy

Oncogene ◽  
2004 ◽  
Vol 23 (23) ◽  
pp. 4136-4145 ◽  
Author(s):  
Ana Preto ◽  
Sim K Singhrao ◽  
Michele F Haughton ◽  
David Kipling ◽  
David Wynford-Thomas ◽  
...  
Keyword(s):  
Cell Death ◽  
Cancer Cells ◽  
Human Cancer ◽  
Growth Arrest ◽  
Wild Type ◽  
Human Cancer Cells ◽  
Wild Type P53 ◽  
Telomere Erosion

scholarly journals Functional Inactivation of Endogenous MDM2 and CHIP by HSP90 Causes Aberrant Stabilization of Mutant p53 in Human Cancer Cells

2011 ◽  
Vol 9 (5) ◽  
pp. 577-588 ◽  
Author(s):  
Dun Li ◽  
Natalia D. Marchenko ◽  
Ramona Schulz ◽  
Victoria Fischer ◽  
Talia Velasco-Hernandez ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Human Cancer ◽  
Mutant P53 ◽  
Human Cancer Cells ◽  
Functional Inactivation

scholarly journals The USP7 Inhibitor P5091 Induces Cell Death in Ovarian Cancers with Different P53 Status

2017 ◽  
Vol 43 (5) ◽  
pp. 1755-1766 ◽  
Author(s):  
Mengying Wang ◽  
Yayun Zhang ◽  
Taishu Wang ◽  
Jinrui Zhang ◽  
Zhu Zhou ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Ovarian Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Pharmacological Intervention ◽  
Ovarian Cancer Cells ◽  
Mutant P53 ◽  
Wild Type ◽  
Ovarian Cancers ◽  
Wild Type P53

Background/Aims: Ovarian cancer is often diagnosed at later stages with poor prognosis. Recent studies have associated the expression of deubiquitylase USP7 with the survival of ovarian cancers. Being a cysteine protease, USP7 could become a target for pharmacological intervention. Therefore, in this study, we assessed the influence of its inhibitor P5091 on ovarian cancer cells. Methods: Ovarian cancer cells were treated with P5091, and cell proliferation was measured with MTT assay; cell morphology was inspected under a phase-contrast microscope; cell cycle and cell death were examined by flow cytometry. To gain mechanistic insights into its effects, immunoblotting was performed to detect USP7, HDM2, p53, p21, apoptosis and autophagy related proteins. Results: P5091 effectively suppressed the growth of ovarian cancer cells, caused cell cycle blockage, and induced necrosis and apoptosis with more severe phenotypes observed in HeyA8 cells with wild-type p53 than in OVCAR-8 cells with mutant p53. P5091 also prompted autophagy, with more efficient p62 degradation in HeyA8. Conclusion: P5091 shows efficacy in suppressing ovarian cancers harbouring wild-type and mutant p53. Its effects seemed to be enhanced by wild-type p53. The potency of this USP7 inhibitor also correlated with autophagy to some extent. Therefore, the pharmacological targeting of USP7 may serve as a potential therapeutic strategy and warrants further investigation.

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