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.
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.
Sioutopoulou
Despina O
DO
Department of Biology and Genetics, Medical School, University of Thessalia, 22 Papakyriazi Street, Larisa 41222, Greece.
Plakokefalos
Elias
E
Arvanitis
Leonidas
L
Athanassiou
Evangelos
E
Venizelos
John
J
Kaplanis
Konstantinos
K
Destouni
Chariclia
C
Nomikos
Iakovos
I
Satra
Maria
M
Vamvakopoulos
Nicholas C
NC
D000230:Adenocarcinoma / Q000235:genetics / Q000378:metabolism / Q000628:therapy / Q000821:virology*; D000956:Antigens, Viral / Q000378:metabolism; D017209:Apoptosis; D002470:Cell Survival; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D015967:Gene Expression Regulation, Viral; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases / Q000235:genetics / Q000378:metabolism; D006367:HeLa Cells; D052161:Human papillomavirus 18 / Q000235:genetics / Q000378:metabolism; D006801:Humans; D009981:Influenza B virus / Q000235:genetics / Q000276:immunology / Q000472:pathogenicity*; D050130:Oncolytic Virotherapy; D050504:Oncolytic Viruses / Q000235:genetics / Q000276:immunology / Q000472:pathogenicity*; D010641:Phenotype; D012333:RNA, Messenger / Q000378:metabolism; D018168:Receptors, Retinoic Acid / Q000235:genetics / Q000378:metabolism; D000072482:Retinoic Acid Receptor alpha; D020133:Reverse Transcriptase Polymerase Chain Reaction; D002583:Uterine Cervical Neoplasms / Q000235:genetics / Q000378:metabolism / Q000628:therapy / Q000821:virology*
D000956:Antigens, Viral; C000607071:RARA protein, human; D012333:RNA, Messenger; D018168:Receptors, Retinoic Acid; D000072482:Retinoic Acid Receptor alpha; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases