Upstream transcription factor 1 prompts malignancies of cervical cancer primarily by transcriptionally activating p65 expression Retraction in /10.3892/etm.2024.12631

Wang,Wen; Yao,Shujuan; Jiang,Hongjing; Dong,Jing; Cui,Xiujuan; Tian,Xiangyu; Guo,Yanyan; Zhang,Shiqian

doi:10.3892/etm.2018.6758

December-2018 Volume 16 Issue 6

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December-2018 Volume 16 Issue 6

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Article Open Access

Upstream transcription factor 1 prompts malignancies of cervical cancer primarily by transcriptionally activating p65 expression

Retraction in: /10.3892/etm.2024.12631

Authors:
- Wen Wang
- Shujuan Yao
- Hongjing Jiang
- Jing Dong
- Xiujuan Cui
- Xiangyu Tian
- Yanyan Guo
- Shiqian Zhang
View Affiliations / Copyright

Affiliations: Department of Obstetrics and Gynecology, Tengzhou Central People's Hospital, Tengzhou, Shandong 277500, P.R. China, Department of Medical Imaging, Tengzhou Central People's Hospital, Tengzhou, Shandong 277500, P.R. China, Department of Obstetrics and Gynecology, Shandong Police Hospital, Jinan, Shandong 250001, P.R. China, Department of Obstetrics and Gynecology, Qilu Hospital, Shandong University, Jinan, Shandong 250012, P.R. China

Copyright: © Wang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
Pages: 4415-4422
|
Published online on: September 18, 2018

https://doi.org/10.3892/etm.2018.6758
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Abstract

Cervical cancer is the third‑most common cause of female cancer‑related mortality worldwide. In cervical cancer, aberrant activation of nuclear factor (NF)‑κB signaling is widely reported. However, the transcriptional regulation of NF‑κB signaling remains unclear. The present study aimed to explore the underlying mechanism in which NF‑κB signaling was activated in cervical cancer cells. Initially, the expression of p65 was demonstrated to be markedly enhanced in grade II, III or IV cervical cancer tissues compared with that of normal cervical tissues, indicating that p65 expression was correlated with tumor grade. In HeLa and CaSki cells, overexpression of p65 markedly enhanced cervical cancer cell invasion and migration. Further experiments demonstrated that p65 overexpression significantly increased the phosphorylation levels of protein kinase B (AKT) and p38. Dual luciferase reporter and chromatin immunoprecipitation assays demonstrated that USF1 was able to bind the promoter region of p65, thereby enhancing the transcriptional activation of p65. Notably, when p65 was silenced, the phosphorylation levels of AKT and p38 were suppressed even in cells transfected with adenovirus vectors expressing upstream transcription factor 1 (USF1). These data indicated that USF1 prompted cervical cancer progression primarily by transcriptionally activating p65. In conclusion, the present study demonstrated that USF1 was able to activate the transcription of p65, thereby enhancing the malignancy of cervical cancer cells.

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