Issue
Copyright (c) 2023 Minjie Fang, Yayan Zhou, Zihuang Li, Xianming Li
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.Transcriptional factor CCAAT enhancer binding protein beta inhibits epithelial-mesenchymal transition in cervical cancer via regulating attractin-like 1
Corresponding Author(s) : Xianming Li
Cellular and Molecular Biology,
Vol. 69 No. 13: Issue 13
Abstract
Cervical cancer (CC) is a malignancy seriously endangering women's life and health worldwide. GEPIA demonstrated that attractin-like 1 (ATRNL1) presents downregulation in CC tissue. Transcription factor CCAAT enhancer binding protein beta (CEBPB) was previously revealed to present depletion in CC tissue. We attempted to clarify molecular mechanism between ATRNL1 and CEBPB underlying CC progression. Bioinformatics, RT-qPCR and western blotting revealed expression characteristics of ATRNL1 in CC. RT-qPCR measured ATRNL1 and CEBPB levels in CC cell lines. Gain-of-function assays clarified role of ATRNL1 in CC cell behaviors. Bioinformatics, Pearson correlation, ChIP and luciferase reporter experiments assessed association of ATRNL1 and CEBPB in CC cells. Rescue assays assessed regulatory function of CEBPB-ATRNL1 in CC cellular processes. ATRNL1 showed depletion in CC tissue and cells at mRNA and protein levels. ATRNL1 upregulation repressed CC cell viability, migration and EMT. CEBPB bound to ATRNL1 promoter to transcriptionally upregulate ATRNL1 in CC cells. The impact of CEBPB elevation on CC cell viability, migration and EMT were countervailed by ATRNL1 depletion. ATRNL1 and CEBPB present depletion and serve as tumor suppressors in CC cells. ATRNL1 suppresses CC cell malignancy through CEBPB activation, which may provide a potential new direction for seeking therapeutic plans for CC.
Keywords
Download Citation
Endnote/Zotero/Mendeley (RIS)BibTeX
