MicroRNA-128 suppresses cell growth and metastasis in colorectal carcinoma by targeting IRS1 Retraction in /10.3892/or.2021.8140

Wu,Lan; Shi,Bo; Huang,Kexin; Fan,Guoyu

doi:10.3892/or.2015.4251

MicroRNA-128 suppresses cell growth and metastasis in colorectal carcinoma by targeting IRS1

Retraction in: /10.3892/or.2021.8140

Authors:
- Lan Wu
- Bo Shi
- Kexin Huang
- Guoyu Fan
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Affiliations: Department of Pediatrics, The First Hospital of Jilin University, Changchun, Jilin 130021, P.R. China, The Experiment Center, College of Basic Medical Sciences, Jilin University, Changchun, Jilin 130021, P.R. China, Department of Oncology, The Center Hospital of Jilin City, Fengman, Jilin 132011, P.R. China
Published online on: September 8, 2015 https://doi.org/10.3892/or.2015.4251
Pages: 2797-2805

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Abstract

Evidence has shown that microRNAs play important roles in tumor development, progression, and metastasis. miR-128 has been reported to be deregulated in different tumor types, whereas the function of miR-128 in colorectal carcinoma (CRC) largely remains to be elucidated. The aim of the present study was to investigate the clinical significance, biological effects and underlying mechanisms of miR-128 in CRC using reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blotting. It was found that the expression of miR-128 was downregulated in CRC tissues and cell lines as determined by RT-qPCR. Furthermore, the expression of miR-128 in tumor tissues was significantly negatively correlated with TNM stage and lymph node metastasis in CRC patients. Functional assay revealed that the overexpression of miR-128 inhibited CRC cell proliferation, colony formation, migration and invasion and promoted apoptosis in vitro, and suppressed CRC xenograft tumor growth in vivo. In addition, insulin receptor substrate 1 (IRS1), a key mediator in oncogenic insulin-like growth factor (IGF) signaling, was confirmed as a direct target of miR-128 by a luciferase reporter assay. Western blot analysis indicated that the overexpression of miR-128 significantly downregulated IRS1 expression and its downstream Akt signaling in CRC cells. Moreover, miR-128 was negatively associated with IRS1 in CRC tissues compared to adjacent non-tumor tissues. Taken together, these data suggested that miR-128 serves as a tumor suppressor and blocks CRC growth and metastasis by targeting IRS1.

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