scholarly journals KPNB1-mediated nuclear import is required for motility and inflammatory transcription factor activity in cervical cancer cells

Oncotarget ◽  
2017 ◽  
Vol 8 (20) ◽  
pp. 32833-32847 ◽  
Author(s):  
Tamara Stelma ◽  
Virna D. Leaner
Keyword(s):  
Cervical Cancer ◽  
Transcription Factor ◽  
Cancer Cells ◽  
Nuclear Import ◽  
Transcription Factor Activity ◽  
Factor Activity ◽  
Cervical Cancer Cells

scholarly journals The Brn-3a transcription factor plays a key role in regulating the growth of cervical cancer cells in vivo

Oncogene ◽  
2001 ◽  
Vol 20 (35) ◽  
pp. 4899-4903 ◽  
Author(s):  
Daniel Ndisang ◽  
Vishwanie Budhram-Mahadeo ◽  
Barbara Pedley ◽  
David S Latchman
Keyword(s):  
Cervical Cancer ◽  
Transcription Factor ◽  
Cancer Cells ◽  
Cervical Cancer Cells

scholarly journals Inhibition of Kpn β 1 Mediated Nuclear Import Enhances Cisplatin Chemosensitivity in Cervical Cancer.

2020 ◽  
Author(s):  
Ru-pin Alicia Chi ◽  
Pauline van der Watt ◽  
Wei Wei ◽  
Michael Birrer ◽  
Virna Leaner
Keyword(s):  
Cervical Cancer ◽  
Cell Death ◽  
Cell Viability ◽  
Cancer Cells ◽  
Combination Treatment ◽  
Nuclear Import ◽  
Reporter Activity ◽  
Cervical Cancer Cells ◽  
Cisplatin Sensitivity ◽  
Pre Treatment

Abstract Background: Inhibition of nuclear import via Karyopherin beta 1 (Kpnβ1) shows potential as an anti-cancer approach. This study investigated the use of nuclear import inhibitor, INI-43, in combination with cisplatin. Methods: Cervical cancer cells were pre-treated with INI-43 before treatment with cisplatin, and MTT cell viability and apoptosis assays performed. Activity and localisation of p53 and NFκB was determined after co-treatment of cells.Results: Pre-treatment of cervical cancer cells with INI-43 at sublethal concentrations enhanced cisplatin sensitivity, evident through decreased cell viability and enhanced apoptosis. Kpnβ1 knock-down cells similarly displayed increased sensitivity to cisplatin. Combination index determination using the Chou-Talalay method revealed that INI-43 and cisplatin engaged in synergistic interactions. p53 was found to be involved in the cell death response to combination treatment as its inhibition abolished the enhanced cell death observed. INI-43 pre-treatment resulted in moderately stabilized p53 and induced p53 reporter activity, which translated to increased p21 and decreased Mcl-1 upon cisplatin combination treatment. Furthermore, cisplatin treatment led to nuclear import of NFκB, which was diminished upon pre-treatment with INI-43. NFκB reporter activity and expression of NFκB transcriptional targets, cyclin D1, c-Myc and XIAP, showed decreased levels after combination treatment compared to single cisplatin treatment and this associated with enhanced DNA damage. Conclusions: Taken together, this study shows that INI-43 pre-treatment significantly enhances cisplatin sensitivity in cervical cancer cells, mediated through stabilization of p53 and decreased nuclear import of NFκB. Hence this study suggests the possible synergistic use of nuclear import inhibition and cisplatin to treat cervical cancer.

scholarly journals Systems analysis of dynamic transcription factor activity identifies targets for treatment in Olaparib resistant cancer cells

2017 ◽  
Vol 114 (9) ◽  
pp. 2085-2095 ◽  
Author(s):  
Joseph T. Decker ◽  
Eric C. Hobson ◽  
Yining Zhang ◽  
Seungjin Shin ◽  
Alexandra L. Thomas ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Cancer Cells ◽  
Systems Analysis ◽  
Transcription Factor Activity ◽  
Factor Activity

scholarly journals Expression of TSG101 protein and LSF transcription factor in HPV-positive cervical cancer cells

2014 ◽  
Vol 7 (5) ◽  
pp. 1409-1413 ◽  
Author(s):  
JUSTYNA K. BRONIARCZYK ◽  
ALICJA WAROWICKA ◽  
ANNA KWAŚNIEWSKA ◽  
MARIA WOHUŃ-CHOLEWA ◽  
WOJCIECH KWAŚNIEWSKI ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Transcription Factor ◽  
Cancer Cells ◽  
Cervical Cancer Cells
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