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

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 Autocrine STAT3 activation in HPV positive cervical cancer through a virus-driven Akt - NF?B - IL-6 signalling axis

2018 ◽  
Author(s):  
Ethan Luc Morgan ◽  
Andrew Macdonald
Keyword(s):  
Cervical Cancer ◽  
Transcription Factor ◽  
Cancer Cells ◽  
Human Keratinocytes ◽  
Hpv Infection ◽  
Primary Human Keratinocytes ◽  
Hpv E6 ◽  
Stat3 Phosphorylation ◽  
Cervical Cancer Cells ◽  
Approved Drugs

Persistent human papillomavirus (HPV) infection is the leading cause of cervical cancer. Although the fundamental link between HPV infection and oncogenesis is established, the specific mechanisms of virus-mediated transformation remain poorly understood. We previously demonstrated that the HPV encoded E6 protein increases the activity of the proto-oncogenic transcription factor STAT3 in primary human keratinocytes; however, the molecular basis for STAT3 activation in cervical cancer remains unclear. Here, we show that STAT3 phosphorylation in HPV positive cervical cancer cells is mediated primarily via autocrine activation by the pro-inflammatory cytokine Interleukin 6 (IL-6). Antibody-mediated blockade of IL-6 signalling in HPV positive cells inhibits STAT3 phosphorylation, whereas both recombinant IL-6 and conditioned media from HPV positive cells leads to increased STAT3 phosphorylation within HPV negative cervical cancer cells. Interestingly, we demonstrate that non-conventional activation of the transcription factor NF?B, involving the protein kinase Akt, is required for IL-6 production and subsequent STAT3 activation. Our data provides new insights into the molecular re-wiring of cancer cells by HPV E6. We reveal that activation of an IL-6 signalling axis drives the autocrine and paracrine phosphorylation of STAT3 within HPV positive cervical cancers cells. Greater understanding of this pathway provides a potential opportunity for the use of existing clinically approved drugs for the treatment of HPV-mediated cervical cancer.

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