On the mechanism of phenotypic conversion of human cervical adenocarcinoma HeLa cells surviving infection by influenza B virus: potential implications for biological management of adenocarcinomas

Despina O Sioutopoulou; Elias Plakokefalos; Leonidas Arvanitis; Evangelos Athanassiou; John Venizelos; Konstantinos Kaplanis; Chariclia Destouni; Iakovos Nomikos; Maria Satra; Nicholas C Vamvakopoulos

doi:10.1016/j.prp.2007.11.010

On the mechanism of phenotypic conversion of human cervical adenocarcinoma HeLa cells surviving infection by influenza B virus: potential implications for biological management of adenocarcinomas

Pathol Res Pract. 2008;204(5):329-34. doi: 10.1016/j.prp.2007.11.010. Epub 2008 Mar 4.

Authors

Despina O Sioutopoulou¹, Elias Plakokefalos, Leonidas Arvanitis, Evangelos Athanassiou, John Venizelos, Konstantinos Kaplanis, Chariclia Destouni, Iakovos Nomikos, Maria Satra, Nicholas C Vamvakopoulos

Affiliation

¹ Department of Biology and Genetics, Medical School, University of Thessalia, 22 Papakyriazi Street, Larisa 41222, Greece.

PMID: 18291599
DOI: 10.1016/j.prp.2007.11.010

Abstract

We infected HeLa cells with low (10(-9) units), medium (10(-6) units), and high (10(-2) units) influenza B titers and compared the resulting human papilloma virus (HPV), retinoic acid receptor alpha subunit (RARalpha) and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) mRNA content of surviving infected hosts with that of their uninfected precursors by semi-quantitative reverse transcriptase/polymerase chain reaction amplification (RT/PCR). This comparison revealed a moderate and drastic dependence of HPV and RARalpha mRNA content, respectively, but a complete independence of GAPDH mRNA expression on viral titer. A mechanism of adoptive replacement of tolerable cellular with viral gene expression was proposed to explain these findings. We conclude that the reported ability of influenza B viruses to specifically target and eliminate the cervical adenocarcinoma HeLa cell line studied may find practical applications in biological cancer management.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Adenocarcinoma / genetics
Adenocarcinoma / metabolism
Adenocarcinoma / therapy
Adenocarcinoma / virology*
Antigens, Viral / metabolism
Apoptosis
Cell Survival
Female
Gene Expression Regulation, Neoplastic
Gene Expression Regulation, Viral
Glyceraldehyde-3-Phosphate Dehydrogenases / genetics
Glyceraldehyde-3-Phosphate Dehydrogenases / metabolism
HeLa Cells
Human papillomavirus 18 / genetics
Human papillomavirus 18 / metabolism
Humans
Influenza B virus / genetics
Influenza B virus / immunology
Influenza B virus / pathogenicity*
Oncolytic Virotherapy*
Oncolytic Viruses / genetics
Oncolytic Viruses / immunology
Oncolytic Viruses / pathogenicity*
Phenotype
RNA, Messenger / metabolism
Receptors, Retinoic Acid / genetics
Receptors, Retinoic Acid / metabolism
Retinoic Acid Receptor alpha
Reverse Transcriptase Polymerase Chain Reaction
Uterine Cervical Neoplasms / genetics
Uterine Cervical Neoplasms / metabolism
Uterine Cervical Neoplasms / therapy
Uterine Cervical Neoplasms / virology*

Substances

Antigens, Viral
RARA protein, human
RNA, Messenger
Receptors, Retinoic Acid
Retinoic Acid Receptor alpha
Glyceraldehyde-3-Phosphate Dehydrogenases