ArticleCellular oncology (Dordrecht, Netherlands)2024
HPV16 E6/E7-mediated regulation of PiwiL1 expression induces tumorigenesis in cervical cancer cells.
Article in Cellular oncology (Dordrecht, Netherlands), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Unraveling the role of PIWI/piRNAs in stem cell therapy: Epigenetic mechanisms and therapeutic potentials.Genes & diseases · 2026Review
- Development of a Double-Antibody Sandwich ELISA for the Detection of HPV16 E6 Protein.Diagnostics (Basel, Switzerland) · 2026Article
- PIWIL genes in hepatocellular carcinoma: a multi-omics approach uncovering dysregulated expression and ceRNA networks in mice.BMC genomic data · 2024Article
- Mechanisms Behind the Impact of PIWI Proteins on Cancer Cells: Literature Review.International journal of molecular sciences · 2024Review
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
purposePiwiL1 has been reported to be over-expressed in many cancers. However, the molecular mechanism by which these proteins contribute to tumorigenesis and their regulation in cancer cells is still unclear. We intend to understand the role of PiwiL1 in tumorigenesis and also its regulation in cervical cells.
methodsWe studied the effect of loss of PiwiL1 function on tumor properties of cervical cancer cells in vitro and in vivo. Also we have looked into the effect of PiwiL1 overexpression in the malignant transformation of normal cells both in vitro and in vivo. Further RNA-seq and RIP-seq analyses were done to get insight of the direct and indirect targets of PiwiL1 in the cervical cancer cells.
resultsHere, we report that PiwiL1 is not only over-expressed, but also play a major role in tumor induction and progression. Abolition of PiwiL1 in CaSki cells led to a decrease in the tumor-associated properties, whereas, its upregulation conferred malignant transformation of normal HaCaT cells. Our study delineates a new link between HPV oncogenes, E6 and E7 with PiwiL1. p53 and E2F1 directly bind and differentially regulate PiwiL1 promoter in a context-dependant manner. Further, RNA-seq together with RIP-RNA-seq suggested a strong and direct role for PiwiL1 in promoting metastasis in cervical cancer cells.
conclusionOur study demonstrates that PiwiL1 act as an oncogene in cervical cancer by inducing tumor-associated properties and EMT pathway. The finding that HPV oncogenes, E6/E7 can positively regulate PiwiL1 suggests a possible mechanism behind HPV-mediated tumorigenesis in cervical cancer.
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