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Copyright (c) 2023 Dong Chen, Huiming You, Xiaoping Xu, Daocheng Liu, Minmin Shen, Yuan Pan, Zhaohui Liu, Lei Zhang, Huijuan Wang
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.MYC-activated CERS6-AS1 sponges miR-6838-5p and regulates the expression of RUBCNL in colorectal cancer
Corresponding Author(s) : Huijuan Wang
Cellular and Molecular Biology,
Vol. 68 No. 12: Issue 12
Abstract
As a leading gastrointestinal malignancy, colorectal cancer (CRC) is a serious threat to people’s health. A great amount of researches have elaborated that long non-coding RNAs (lncRNAs) play a key role in all kinds of tumors. In the current study, we mainly probed into the mechanisms of CERS6 antisense RNA 1 (CERS6-AS1) underlying CRC. For this purpose, the CERS6-AS1 expression level in CRC cells was disclosed by quantitative real-time PCR (qRT-PCR). In vitro and in vivo assays have validated the functional role of CERS6-AS1 in CRC. Mechanism assays were carried out to confirm the potential mechanism of CERS6-AS1 in CRC. Results showed that through experiments, we identified that the CERS6-AS1 expression level was up-regulated in CRC and the depletion of CERS6-AS1 hindered cell proliferative and migratory abilities and stimulated cell apoptotic levels in CRC. In addition, silencing of CERS6-AS1 repressed tumor growth. Moreover, CERS6-AS1 activated by MYC could sequestermiR-6838-5p, and then regulate rubicon-like autophagy enhancer (RUBCNL) expression level to influence the CRC cell proliferation, migration and apoptosis. In conclusion, The study focused on the MYC/CERS6-AS1/miR-6838-5p/RUBCNL axis was helpful for the potential diagnosis and standardized treatment of CRC.
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