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Investigation of the Expression Level of Human Endogenous Retrovirus E Env Transcript in Cervical Cancer Publisher Pubmed



Jahanshahi S ; Soleimanijelodar R ; Jalilvand S ; Shoja Z ; Farahmand M ; Arashkia A ; Marashi SM
Authors

Source: Retrovirology Published:2026


Abstract

Although HPV infection is obligatory for almost all cases of cervical cancer (CC), other risk factors can promote the progression of cervical cancer. In this context, the expression of human endogenous retroviruses (HERVs) in the development of CC has been investigated. In this study, the expression status of HERV-E env transcripts was analyzed in 111 cervical biopsies, including 35 cervical cancer samples, 20 precancerous lesions, and 56 normal samples. Real-time PCR with specific primers was used to quantify the relative expression of HERV-E env, HPV 16 and 18 E6/E7 genes, and GAPDH as a normalization control. Our results indicated an increase in the expression of HERV-E env, and the difference was statistically significant in the cancer group compared to the precancerous group (1.5-fold change) (P = 0.031). In HPV 16 or 18-infected patients, a higher mean value of HERV-E env mRNA was also found in the cancer group than in the precancerous group. ROC curve analysis showed a significant difference in env expression between precancerous and cancerous lesions in all patients analyzed (P = 0.015) and in a group of patients infected with HPV 16 or 18 genotypes (P = 0.023). In addition, there was a positive correlation between the higher expression of HERV-E env mRNA with E7 (R = 0.34, P = 0.016) and age (R = 0.35, p = 0.016) in HPV 16-infected patients. In conclusion, our study found a possible association between HERV-E env expression and cervical cancer, as HERV-E is actively transcribed during the progression of cervical lesions. Future studies on the potential interaction of HERV-E env with HPV 16 E7 oncoprotein are likely to elucidate common signaling pathways in the progression of cervical cancer and other HPV-related malignancies. © The Author(s) 2026.
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