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. 2018 May 18;8:7840. doi: 10.1038/s41598-018-26292-w

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Schematic diagram explaining the mechanism of CSC maintenance in cervical cancer via let-7i-5p, miR-181a-2-3p and EGF/PI3K/SOX2 axis. In this study, it was observed that exogenous EGF added to the media used for CSC enrichment induces the expression of PI3K and phosphorylates AKT, leading to the enhanced expression of SOX2. SOX2 silencing drastically reduced the CSC population in CaSki cells. The inhibition of EGFR phosphorylation and PI3K reduced the expression of SOX2 and subsequently suppressed the CSC population, thereby establishing the role of EGF pathway in the maintenance of cervical CSCs. While EGF pathway promotes CSC maintenance, let-7i-5p and miR-181a-2-3p counteracts by indirectly targeting SOX2 and thereby suppressing the cervical CSCs. let-7i-5p inhibits HMGA2 (an inducer of SOX2 expression) and miR-181a-2-3p inhibits PI3kinase p55γ (PI3K activator). Hence, activation of EGF pathway and inhibition of let-7i-5p and miR-181a-2-3p are vital for cervical CSC maintenance. The reported literature suggests that HPV infection may cause activation of EGF pathway. If proven, this would perhaps explain the formation of cervical CSCs and hence the origin of cervical cancer.