Abstract

Unexpected inhibition of cervical carcinoma cell proliferation by expression of heat shock transcription factor 1

Highlights

  • Cervical carcinoma incidence is increasing in incidence each year in the world, among young women

  • In order to identify the roles of Heat shock transcription factor 1 (HSF1) in cervical carcinoma, we established HeLa cell lines inducibly expressing constitutively active HSF1 (Figure 1A, upper panel)

  • We picked up three clones from each line and found the growth of constitutively active HSF1 (caHSF1)-carrying cells was prominently suppressed when caHSF1 was inducibly expressed by tetracycline withdrawal

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Summary

Introduction

Cervical carcinoma incidence is increasing in incidence each year in the world, among young women. It is widely known that human papillomaviruses (HPV) are significant risk factor for the development of cervical carcinoma [1,2]. HeLa is a cervical carcinoma cell line that has contributed to the various fields of research including cancer. It has been discovered that the p53 tumor suppressor pathway has been disrupted by HPV in these cell lines including HeLa and 90% of cervical carcinoma cells. P53 protein is known to be actively degraded by HPV E6 protein and stabilization and activation of p53 is suppressed. These reactions normally occur in response to HPV E7 oncogene oncoprotein expression [4,5,6,7]

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