期刊
INTERNATIONAL JOURNAL OF ONCOLOGY
卷 53, 期 2, 页码 579-591出版社
SPANDIDOS PUBL LTD
DOI: 10.3892/ijo.2018.4432
关键词
human papillomavirus type 16-E7; 17-oestradiol; microarrays; carcinogenesis; K14E7; Granzyme B
类别
资金
- Institute of Science and technology of Mexico City [PICSA10-190, 326/2011]
- National Council for Science and Technology [168896]
- Sectorial Funding for Research in Health and Social Security [261875]
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 17-oestradiol (E-2) 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 E-2. 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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