Human papillomavirus type 16 E7 promotes cell viability and migration in cervical cancer by regulating the miR-23a/HOXC8 axis
Background Human papillomavirus (HPV) is a risk factor for the occurrence of cervical cancer (CC). Here, we aimed to explore the role of HPV16 in CC and identify the underlying mechanism.Methods The expression of miR-23a, HPV16 E6/E7 and homeobox C8 (HOXC8) was measured by quantitative real-time PCR...
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| Format: | Article |
| Language: | English |
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Taylor & Francis Group
2024-12-01
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| Series: | Journal of Obstetrics and Gynaecology |
| Subjects: | |
| Online Access: | https://www.tandfonline.com/doi/10.1080/01443615.2024.2311658 |
| _version_ | 1826893649325064192 |
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| author | Yahang Chen Lei Sun Lin Li |
| author_facet | Yahang Chen Lei Sun Lin Li |
| author_sort | Yahang Chen |
| collection | DOAJ |
| description | Background Human papillomavirus (HPV) is a risk factor for the occurrence of cervical cancer (CC). Here, we aimed to explore the role of HPV16 in CC and identify the underlying mechanism.Methods The expression of miR-23a, HPV16 E6/E7 and homeobox C8 (HOXC8) was measured by quantitative real-time PCR or western blot. Cell viability and migration were evaluated using cell counting kit-8, Transwell and wound healing assays. The targeting relationship between miR-23a and HOXC8 was revealed by dual-luciferase reporter assay.Results miR-23a was downregulated in HPV16-positive (HPV16+) CC tissues and HPV16+ and HPV18+ cells. Additionally, E6/E7 expression was increased in CC cells. Then, we found that E7, rather than E6, positively regulated miR-23a expression. miR-23a suppressed cell viability and migration, whereas E7 overexpression abrogated this suppression. miR-23a targeted HOXC8, which reversed miR-23a-mediated cell viability and migration.Conclusions HPV16 E7-mediated miR-23a suppressed CC cell viability and migration by targeting HOXC8, suggesting a novel mechanism of HPV-induced CC. |
| first_indexed | 2024-03-08T03:03:55Z |
| format | Article |
| id | doaj.art-658a5b677ba441c899a1145c4b930189 |
| institution | Directory Open Access Journal |
| issn | 0144-3615 1364-6893 |
| language | English |
| last_indexed | 2025-02-17T04:57:25Z |
| publishDate | 2024-12-01 |
| publisher | Taylor & Francis Group |
| record_format | Article |
| series | Journal of Obstetrics and Gynaecology |
| spelling | doaj.art-658a5b677ba441c899a1145c4b9301892025-01-09T12:13:17ZengTaylor & Francis GroupJournal of Obstetrics and Gynaecology0144-36151364-68932024-12-0144110.1080/01443615.2024.2311658Human papillomavirus type 16 E7 promotes cell viability and migration in cervical cancer by regulating the miR-23a/HOXC8 axisYahang Chen0Lei Sun1Lin Li2Department of Gynecology, Heilongjiang Provincial Hospital, Harbin, ChinaDepartment of Obstetrics and Gynecology, Shuangcheng District People’s Hospital, Harbin, ChinaDepartment of Gynecology, Heilongjiang Provincial Hospital, Harbin, ChinaBackground Human papillomavirus (HPV) is a risk factor for the occurrence of cervical cancer (CC). Here, we aimed to explore the role of HPV16 in CC and identify the underlying mechanism.Methods The expression of miR-23a, HPV16 E6/E7 and homeobox C8 (HOXC8) was measured by quantitative real-time PCR or western blot. Cell viability and migration were evaluated using cell counting kit-8, Transwell and wound healing assays. The targeting relationship between miR-23a and HOXC8 was revealed by dual-luciferase reporter assay.Results miR-23a was downregulated in HPV16-positive (HPV16+) CC tissues and HPV16+ and HPV18+ cells. Additionally, E6/E7 expression was increased in CC cells. Then, we found that E7, rather than E6, positively regulated miR-23a expression. miR-23a suppressed cell viability and migration, whereas E7 overexpression abrogated this suppression. miR-23a targeted HOXC8, which reversed miR-23a-mediated cell viability and migration.Conclusions HPV16 E7-mediated miR-23a suppressed CC cell viability and migration by targeting HOXC8, suggesting a novel mechanism of HPV-induced CC.https://www.tandfonline.com/doi/10.1080/01443615.2024.2311658Cervical cancerhuman papillomavirus type 16 E7HOXC8miRNA-23a |
| spellingShingle | Yahang Chen Lei Sun Lin Li Human papillomavirus type 16 E7 promotes cell viability and migration in cervical cancer by regulating the miR-23a/HOXC8 axis Journal of Obstetrics and Gynaecology Cervical cancer human papillomavirus type 16 E7 HOXC8 miRNA-23a |
| title | Human papillomavirus type 16 E7 promotes cell viability and migration in cervical cancer by regulating the miR-23a/HOXC8 axis |
| title_full | Human papillomavirus type 16 E7 promotes cell viability and migration in cervical cancer by regulating the miR-23a/HOXC8 axis |
| title_fullStr | Human papillomavirus type 16 E7 promotes cell viability and migration in cervical cancer by regulating the miR-23a/HOXC8 axis |
| title_full_unstemmed | Human papillomavirus type 16 E7 promotes cell viability and migration in cervical cancer by regulating the miR-23a/HOXC8 axis |
| title_short | Human papillomavirus type 16 E7 promotes cell viability and migration in cervical cancer by regulating the miR-23a/HOXC8 axis |
| title_sort | human papillomavirus type 16 e7 promotes cell viability and migration in cervical cancer by regulating the mir 23a hoxc8 axis |
| topic | Cervical cancer human papillomavirus type 16 E7 HOXC8 miRNA-23a |
| url | https://www.tandfonline.com/doi/10.1080/01443615.2024.2311658 |
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