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Copyright (c) 2025 Zhimin Liu, Yiping Li, Shangkui Xie , Donglin Ren, Dandan Huang
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.MiR-200b-3p is involved in colorectal cancer progression by targeting DDIT4
Corresponding Author(s) : Dandan Huang
Cellular and Molecular Biology,
Vol. 71 No. 11: Issue 11
Abstract
This study aimed to explore the functional dynamics between microRNA-200b-3p (miR-200b-3p) and DNA damage-induced transcript 4 (DDIT4) in colorectal cancer (CRC) and their potential as therapeutic targets. Pan-cancer analysis was conducted to evaluate DDIT4 expression across multiple cancer types. Immunohistochemical staining of CRC clinical samples was performed to confirm DDIT4 protein levels. Functional assays, including cell proliferation, migration, and invasion analyses, were used to assess the effects of DDIT4 silencing in CRC cells. Bioinformatics and experimental validation identified microRNAs targeting DDIT4 and their prognostic significance using GEPIA, HPA and ENCORI databases. Pan-cancer analysis showed DDIT4 was highly expressed in CRC compared to other cancers. Immunohistochemistry confirmed moderate to high DDIT4 expression in CRC patient samples. Knockdown of DDIT4 significantly reduced proliferation, migration, and invasion of SW480 CRC cells. miRNA analysis identified miR-200b-3p as a potential regulator of DDIT4. Low expression of miR-200b-3p correlated with poor prognosis in CRC patients. Luciferase reporter assays confirmed direct binding of miR-200b-3p to DDIT4 mRNA. Furthermore, overexpression of DDIT4 was shown to mitigate the tumor-suppressive effects of miR-200b-3p, restoring proliferation, migration, and invasion. DDIT4 promotes CRC progression and is regulated by miR-200b-3p. Targeting the miR-200b-3p/DDIT4 axis may represent a novel therapeutic approach for CRC treatment.
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