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Int J Oncol. 2018 Aug;53(2):579-591. doi: 10.3892/ijo.2018.4432. Epub 2018 Jun 6.

Early synergistic interactions between the HPV16‑E7 oncoprotein and 17β-oestradiol for repressing the expression of Granzyme B in a cervical cancer model.

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Department of Genetics and Molecular Biology, Centre for Research and Advanced Studies of the National Polytechnic Institute, México City 07360, México.
Biomedical Unit for Cancer Research, National Autonomous University of Mexico/National Institute of Cancer, México City 14080, México.
Laboratory of Cell and Developmental Signalling, National Cancer Institute at Frederick, Frederick, MD 21702, USA.
Research Unit of Genetics and Cancer, Juárez Hospital, México City 07760, México.
Department of Oncogenomics, National Institute of Genomic Medicine, México City 14610, México, México.
Department of Oncology, Lombardi Comprehensive Cancer Centre, Georgetown University Medical Centre, Washington, DC 20057, USA.
McArdle Laboratory for Cancer Research, University of Wisconsin School of Medicine and Public Health, Madison, WI 53706, USA.


Although high-risk human papillomavirus (HR‑HPV) infection has a prominent role in the aetiology of cervical cancer (CC), sex steroid hormones may also be involved in this process; however, the cooperation between oestrogen and HR‑HPV in the early stages of cervical carcinogenesis is poorly understood. Since 17β-oestradiol (E2) and the HPV type 16‑E7 oncoprotein induce CC in transgenic mice, a microarray analysis was performed in the present study to generate global gene expression profiles from 2‑month‑old FVB (non‑transgenic) and K14E7 (transgenic) mice who were left untreated or were treated for 1 month with E2. Upregulation of cancer-related genes that have not been previously reported in the context of CC, including glycerophosphodiester phosphodiesterase domain containing 3, interleukin 1 receptor type II, natriuretic peptide type C, MGAT4 family member C, lecithin-retinol acyltransferase (phosphatidylcholine-retinol-O-acyltransferase) and glucoside xylosyltransferase 2, was observed. Notably, upregulation of the serine (or cysteine) peptidase inhibitor clade B member 9 gene and downregulation of the Granzyme gene family were observed; the repression of the Granzyme B pathway may be a novel mechanism of immune evasion by cancer cells. The present results provide the basis for further studies on early biomarkers of CC risk and synergistic interactions between HR‑HPV and oestrogen.

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