Susceptibility of epithelial cells cultured from different regions of human cervix to HPV16-induced immortalization

PLoS One. 2018 Jun 26;13(6):e0199761. doi: 10.1371/journal.pone.0199761. eCollection 2018.

Abstract

Persistent infection with high-risk human papillomavirus (HPV) is a major risk factor for cervical cancer. Greater than 90% of these cancers originate in the cervical transformation zone (TZ), a narrow region of metaplastic squamous epithelium that develops at the squamocolumnar junction between the ectocervix and endocervix. It is unclear why the TZ has high susceptibility to malignant transformation and few studies have specifically examined cells from this region. We hypothesized that cells cultured from TZ are more susceptible to cellular immortalization, an alteration that contributes to malignant development. We cultured primary epithelial cells from each region of human cervix (ectocervix, endocervix and TZ) and measured susceptibility to immortalization after transfection with the complete HPV-16 genome or infection of HPV16 E6/E7 retroviruses. Cells cultured from each cervical region expressed keratin markers (keratin 14 and 18) that confirmed their region of origin. In contrast to our prediction, cells from TZ were equally susceptible to immortalization as cells from ectocervix or endocervix. Thus, increased susceptibility of the TZ to cervical carcinogenesis is not due to increased frequency of immortalization by HPV-16. We developed a series of HPV16-immortalized cell lines from ectocervix, endocervix and TZ that will enable comparisons of how these cells respond to factors that promote cervical carcinogenesis.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Transformation, Viral*
  • Cells, Cultured
  • Cervix Uteri* / metabolism
  • Cervix Uteri* / pathology
  • Cervix Uteri* / virology
  • Epithelial Cells* / metabolism
  • Epithelial Cells* / pathology
  • Epithelial Cells* / virology
  • Female
  • Human papillomavirus 16 / metabolism*
  • Humans
  • Papillomavirus Infections* / metabolism
  • Papillomavirus Infections* / pathology
  • Uterine Cervical Neoplasms* / metabolism
  • Uterine Cervical Neoplasms* / pathology
  • Uterine Cervical Neoplasms* / virology

Grants and funding

This work was funded by an award from the National Cancer Institute 1R15CA173703-01 (CDW) and by an award from US Biomax, Inc (CDW). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.