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miR-5191 functions as a tumor suppressor by targeting RPS6KB1 in colorectal cancer

Authors
An, Hyun-JuPark, MisunKim, JoonHan, Young-Hoon
Issue Date
10월-2019
Publisher
SPANDIDOS PUBL LTD
Keywords
microRNA; microRNA-5191; colorectal cancer; ribosomal protein S6 kinase beta 1; apoptosis
Citation
INTERNATIONAL JOURNAL OF ONCOLOGY, v.55, no.4, pp.960 - 972
Indexed
SCIE
SCOPUS
Journal Title
INTERNATIONAL JOURNAL OF ONCOLOGY
Volume
55
Number
4
Start Page
960
End Page
972
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/62684
DOI
10.3892/ijo.2019.4865
ISSN
1019-6439
Abstract
MicroRNAs (miRNAs/miRs) are a class of small non-coding RNAs that play pivotal roles in cancer physiology as important epigenetic regulators of gene expression. Several miRNAs have been previously discovered that regulate the proliferation of the colorectal cancer (CRC) cell line HCT116. In the present study, one of these miRNAs, miR-5191, was characterized as a tumor suppressor in CRC cells. Transfection with miR-5191 led to a significant decrease in cell proliferation, invasiveness, tumor sphere-forming ability and tumor organoid growth, as determined via trypan blue, Transwell, sphere culture and organoid culture assays, respectively. Flow cytometric analyses revealed that miR-5191 induced the cell cycle arrest and apoptosis of CRC cells. Additionally, the expression of miR-5191 was downregulated in CRC tumor tissues compared with in normal tissues, as measured by reverse transcription-quantitative PCR analysis. Ribosomal protein S6 kinase beta 1 (RPS6KB1) was identified as a direct target of miR-5191. Ectopic expression of RPS6KB1 suppressed the function of miR-5191. Intratumoral injection of miR-5191 mimic suppressed tumor growth in HCT116 xeno-grafts. These findings suggested a novel tumor-suppressive function for miR-5191 in CRC, and its potential applicability for the development of anticancer miRNA therapeutics.
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