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Elevated miR-16-5p induces somatostatin receptor 2 expression in neuroendocrine tumor cells

Authors
 HanHee Jo  ;  Yusun Park  ;  Jisu Kim  ;  Hyeonjeong Kwon  ;  Taehun Kim  ;  JongSook Lee  ;  Jae-Chul Pyun  ;  Misu Lee  ;  Mijin Yun 
Citation
 PLOS ONE, Vol.15(10) : e0240107, 2020-10 
Journal Title
 PLOS ONE 
Issue Date
2020-10
Abstract
Somatostatin analogs, which are used to treat neuroendocrine tumors, inhibit hormone secretion or promote tumor shrinkage; however, their efficacy varies between patients, possibly because of differential expression of somatostatin receptors (SSTRs) in tumors. In this study, we evaluated the regulatory mechanism underlying the expression of SSTR2, the main octreotide target. Thirty miRNAs were found to be dysregulated in neuroendocrine cells (INS-1 cells) incubated with octreotide compared to that in placebo-treated cells. Among the upregulated miRNAs, miR-16-5p was elevated after short-term octreotide treatment. We conducted in vitro experiments to determine whether the expression of miR-16-5p was associated with the regulation of SSTR2 expression and affected octreotide sensitivity in INS-1 cells. Overexpression of miR-16-5p by transfected mimics induced upregulation of SSTR2 expression. Additionally, the expression of miR-16-5p further enhanced octreotide-induced reduction in cell proliferation in both two- and three-dimensional culture of INS-1 cells. Thus, our results reveal the mechanism underlying SSTR2 expression regulation and may aid in developing therapeutic approaches for enhancing the response to octreotide, particularly in patients unresponsive to SSTR2-targeted somatostatin analog treatment.
Files in This Item:
T202004173.pdf Download
DOI
10.1371/journal.pone.0240107
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Nuclear Medicine (핵의학교실) > 1. Journal Papers
Yonsei Authors
Yun, Mi Jin(윤미진) ORCID logo https://orcid.org/0000-0002-1712-163X
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/180142
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