ISSN: 1948-5964
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Laboratory of Molecular Virology, Department of Biological Sciences, The Dedman College Center for Drug Discovery, Design and Delivery, Southern Methodist University, Dallas, Texas, 75275-0376, United States
Robert Harrod works at Laboratory of Molecular Virology, Department of Biological Sciences, The Dedman College Center for Drug Discovery, Design & Delivery, Southern Methodist University, Dallas, Texas, 75275-0376, USA
Research Article
siRNA-Inhibition of TIGAR Hypersensitizes Human Papillomavirus-Transformed Cells to Apoptosis Induced by Chemotherapy Drugs that Cause Oxidative Stress
Author(s): Lacin Yapindi, Brenda Y. Hernandez and Robert Harrod*
The high-risk subtype Human Papillomaviruses (hrHPVs), including HPV16, HPV18, HPV31, HPV33, and HPV45,
infect and oncogenically transform epithelial cells and cause squamous cell carcinomas and adenocarcinomas
associated with the development of cervical cancer and subsets of vulvar, vaginal, penile, and anogenital cancers,
as well as head-and-neck oropharyngeal carcinomas which often have poor clinical prognoses. Many cancers have
been shown to contain elevated levels of the TP53-Induced Glycolysis and Apoptosis Regulator (TIGAR)-a glycolytic
enzyme and antioxidant effector which frequently correlates with an aggressive tumor phenotype and serves as a
determinant of therapy-resistance. We therefore tested whether siRNA-inhibition of TIGAR protein expression
could sensitize HPV18-transformed HeLa cells to genotoxic chemotherapy agents (i.e., cisplatin, etoposide,
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DOI:
10.35248/1948-5964.21.13.223