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Copyright (c) 2022 Tingting Gu, Huafeng Pan, Fei Zhang, Li Wang, Zhongliang Cheng
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
The undersigned hereby assign all rights, included but not limited to copyright, for this manuscript to CMB Association upon its submission for consideration to publication on Cellular and Molecular Biology. The rights assigned include, but are not limited to, the sole and exclusive rights to license, sell, subsequently assign, derive, distribute, display and reproduce this manuscript, in whole or in part, in any format, electronic or otherwise, including those in existence at the time this agreement was signed. The authors hereby warrant that they have not granted or assigned, and shall not grant or assign, the aforementioned rights to any other person, firm, organization, or other entity. All rights are automatically restored to authors if this manuscript is not accepted for publication.The FOXP4-AS1/miR-3130-3p/SP4 feedback loop is associated with prostate cancer
Corresponding Author(s) : Zhongliang Cheng
Cellular and Molecular Biology,
Vol. 68 No. 10: Issue 10
Abstract
The vital function of mounting long noncoding RNAs (lncRNAs) in prostate cancer (PCa) has been illustrated in increasing reports. However, the roles of many lncRNAs in PCa have not been deciphered. A total of 62 pairs of PCa and adjacent normal tissue samples were provided by PCa patients undergoing surgery. Extensive assays were conducted in this study to investigate the role of FOXP4 antisense RNA 1 (FOXP4-AS1) in PCa tumorigenesis. This study elucidated that FOXP4-AS1 expression was elevated in PCa tissue samples and cell lines. Loss-of-function experiments revealed that depleted FOXP4-AS1 inhibited PCa cell proliferation in vitro and retarded tumor growth in vivo. Mechanically, FOXP4-AS1 functioned as a competing endogenous RNA (ceRNA) of miR-3130-3p, releasing SP4 from the inhibitory effect of miR-3130-3p. Rescue assays validated that FOXP4-AS1 modulated PCa progression via SP4. Interestingly, SP4 is known as a transcription factor and was predicted to bind with the promoter region of FOXP4-AS1. This current research confirmed that SP4 activated the transcription activity of FOXP4-AS1 and thus positively regulated its expression. To conclude, we discovered that FOXP4-AS1, miR-3130-3p, and SP4 constitute a feedback loop and contribute to PCa tumorigenesis, providing a new valuable diagnosis and therapeutic strategy for PCa.
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