MicroRNA‑101 suppresses colorectal cancer progression by negative regulation of Rap1b
- Zhiyuan Zhou
- Hang Xu
- Yantao Duan
- Bin Liu
Affiliations: Department of General Surgery, Shanghai Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200011, P.R. China
- Published online on: July 1, 2020 https://doi.org/10.3892/ol.2020.11791
Copyright: © Zhou
et al. This is an open access article distributed under the
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Colorectal cancer (CRC) is the fourth most lethal malignancy and is the second most common cause of cancer‑associated mortality worldwide. The development of high‑throughput sequencing has enabled the identification of potential biomarkers for the diagnosis and treatment of various types of cancer. Although microRNA‑101 (miR‑101) has been demonstrated to be a potential biomarker of CRC, its detailed mechanisms remain to be fully discovered. In the present study, overall survival analysis was applied to determine the association between miR‑101 and CRC prognosis. Reverse transcription‑quantitative PCR (RT‑qPCR) was used to examine gene expression levels in tissues and cells. Cell proliferative and apoptotic activities were determined by MTT and flow cytometry assays, respectively. Wound healing and Transwell assays were used to examine CRC cell migration and invasion, respectively. In the present study, RT‑qPCR analysis indicated that miR‑101 was significantly downregulated in CRC tissues and cells. However, clinical data collected from The Cancer Genome Atlas revealed no significant association between the expression levels of miR‑101 and the prognosis of CRC. Additionally, miR‑101 inhibited the progression of CRC by directly binding to the 3'‑untranslated region of Ras‑related protein Rap1b (Rap1b). This was associated with downregulation of Rap1b expression. Furthermore, the overexpression of Rap1b promoted miR‑101 mimic‑attenuated CRC cell progression. The present study demonstrated that miR‑101 may be involved in the repression of the CRC progression by forming a negative feedback loop with Rap1b. The findings revealed the interaction between miR‑101 and Rap1b during the progression of CRC, which could aid the development of therapeutic strategies.