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Copyright (c) 2022 Cuipeng Zhang, Jing Wang, Hongwei Wang, Jing 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.Circ-ABCC1 enhances radioresistance of breast cancer cells via miR-627-5p/ABCC1 axis
Corresponding Author(s) : Cuipeng Zhang
Cellular and Molecular Biology,
Vol. 68 No. 10: Issue 10
Abstract
Adjuvant radiotherapy represents the standard of care for breast cancer (BC) following breast-conserving surgery. Tumor recurrence after radiotherapy, attributed to acquired radioresistance, has been a haunting and intractable problem. Therefore, preventions from tumor recurrence are vital for improving survival. Recent evidence has suggested circular RNAs (circRNAs) play a part in regulating the radioresistance of varied cancers, including BC. This research concentrated on a novel circRNA hsa_circ_0003427 (termed as circ-ABCC1), probing its influence on the radio-resistance of BC cells, together with the latent molecular mechanism. For this aim, CCK-8 and colony formation assays monitored the changes in viability and proliferation of radio-resistant BC cells. Caspase-3 activity was examined to evaluate cell apoptosis. Bioinformatics prediction and mechanistic assays were involved to determine RNA interactions. Results showed that Circ-ABCC1 was found to be significantly up-regulated in radio-resistant BC cells, in comparison with the corresponding parental BC cells. As to molecular mechanism, circ-ABCC1 served as the miR-627-5p decoy, consequently increasing ABCC1 expression. Rescue assays uncovered that the suppressive impact of circ-ABCC1 silence on BC cell radio-resistance was allowed to be antagonized by miR-627-5p inhibition or ABCC1 up-regulation. In conclusion, Circ-ABCC1 aggravates the radioresistance of BC cells by targeting the miR-627-5p/ABCC1 axis.
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