MicroRNA-155 enhances the activation of Wnt/β-catenin signaling in colorectal carcinoma by suppressing HMG-box transcription factor 1 Retraction in /10.3892/mmr.2022.12597

Wan,Ying‑Chun; Li,Tao; Han,Yang‑Dong; Zhang,Hai‑Yan; Lin,Hai; Zhang,Bin

doi:10.3892/mmr.2016.4788

MicroRNA-155 enhances the activation of Wnt/β-catenin signaling in colorectal carcinoma by suppressing HMG-box transcription factor 1

Retraction in: /10.3892/mmr.2022.12597

Authors:
- Ying‑Chun Wan
- Tao Li
- Yang‑Dong Han
- Hai‑Yan Zhang
- Hai Lin
- Bin Zhang
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Affiliations: Department of Endocrinology, China‑Japan Union Hospital, Jilin University, Changchun, Jilin 130033, P.R. China, Department of Anesthesiology, China‑Japan Union Hospital, Jilin University, Changchun, Jilin 130033, P.R. China, Department of Gastrointestinal Surgery, China‑Japan Union Hospital, Jilin University, Changchun, Jilin 130033, P.R. China, Department of Internal Medicines, Outpatient Department, Aviation University of Air Force, Jilin University, Changchun, Jilin 130033, P.R. China, Microscopic Examination Department, China‑Japan Union Hospital, Jilin University, Changchun, Jilin 130033, P.R. China
Published online on: January 15, 2016 https://doi.org/10.3892/mmr.2016.4788
Pages: 2221-2228

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Abstract

Colorectal carcinoma (CRC) is a malignant solid tumor arising from the large intestine and is associated with an increasing incidence and poor prognosis. Further understanding of the molecular mechanisms underlying CRC may contribute to the development of novel effective therapeutic strategies. MicroRNAs (miRs), including miR‑155, have been reported to be associated with the etiology and biology of CRC; however, the molecular mechanisms by which miR‑155 affect CRC remain to be fully elucidated. The present study used a multidisciplinary approach, involving reverse transcription‑quantitative polymerase chain reaction, northern blotting, MTT assay, cell cycle progression analysis, immunoblotting, and animal experiments, to determine the possible targets of miR‑155 in CRC cells. miR‑155 was found to be overexpressed in CRC tissue samples, compared with paired normal colon tissue samples. In addition, the inhibition of miR‑155 induced a deceleration in CRC cell proliferation and inactivation of the Wnt/β‑catenin signaling pathway. miR‑155 suppression also reduced the growth of CRC xenografts in an animal model. HMG‑box transcription factor 1 (HBP1) was identified as a novel target of miR‑155, which mediated its effect on CRC via the Wnt/β‑catenin pathway. Furthermore, patients with CRC exhibiting higher serum levels of miR‑155 exhibited reduced survival rates. In conclusion, the present study demonstrated that miR‑155 may contribute to the progression and growth of CRC by enhancing the Wnt/β‑catenin pathway in an HBP1‑associated mechanism. Therefore, miR‑155 may be considered a promising therapeutic target for the treatment of CRC.

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