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Copyright (c) 2023 Zongyu Xia, Qin Wang, Peng Lu
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.LncRNA LINC00885 promotes bladder cancer progression by targeting the miR-98-5p/PBX3 axis
Corresponding Author(s) : Peng Lu
Cellular and Molecular Biology,
Vol. 69 No. 3: Issue 3
Abstract
Depicted as the most prevalent malignancy, bladder cancer (BLCA) associated deaths in males all around the world. Increasing evidence has uncovered that dysregulation of lncRNA is associated with the complex processes of various tumors. Although recent research concerning bladder cancer has mentioned the participation of lncRNALINC00885, the specific regulatory role of LINC00885 in BLCA hasn’t been elucidated. This study aimed to explore the regulatory role of LINC00885 in BLCA. For this purpose, qRT-PCR checked the LINC00885 expression. CCK-8, caspase-3, colony formation, and western blot (WB) experiments were carried out to intestate LINC00885 specific role in BLCA. RIP and RNA pull-down assays were used to study the regulation effect between miR-98-5p and LINC00885 (or PBX3) in BLCA. Results showed that LINC00885 was up-regulated in BLCA and promoted cell proliferation, inhibited cell apoptosis in BLCA. Molecular mechanism experiments displayed that miR-98-5p could bind to LINC00885 and PBX3. Up-regulated miR-98-5p reduced cell proliferation, and facilitated cell apoptosis in BLCA. Besides, miR-98-5p could down-regulated PBX3 expression while LINC0088 could up-regulate PBX3 in BLCA. Final rescue tests demonstrated that PBX3 deficiency reversed the miR-98-5p inhibition effect on the progression of sh-LINC00885#1-transfected cells. In conclusion, LINC00885 enhances BLCA progression by targeting the miR-98-5p/PBX3 axis, revealing that LINC00885 might serve as a novel molecular marker in bladder cancer treatment.
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