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Elevated miR-16-5p induces somatostatin receptor 2 expression in neuroendocrine tumor cells
by
Lee, JongSook
, Yun, Mijin
, Jo, HanHee
, Kim, Taehun
, Pyun, Jae-Chul
, Lee, Misu
, Kwon, Hyeonjeong
, Kim, Jisu
, Park, Yusun
in
Analogs
/ Animals
/ Antineoplastic Agents, Hormonal - pharmacology
/ Apoptosis
/ Bioengineering
/ Biology and life sciences
/ Cancer
/ Care and treatment
/ Cell culture
/ Cell Line, Tumor
/ Cell proliferation
/ Development and progression
/ Gene expression
/ Gene Expression Regulation, Neoplastic - drug effects
/ Genetic aspects
/ Health aspects
/ HeLa Cells
/ Hormone receptors
/ Hormones
/ Humans
/ Laboratories
/ Life sciences
/ Materials science
/ Medicine and Health Sciences
/ MicroRNA
/ MicroRNAs
/ MicroRNAs - genetics
/ Neuroendocrine Cells - drug effects
/ Neuroendocrine Cells - metabolism
/ Neuroendocrine Cells - pathology
/ Neuroendocrine tumors
/ Neuroendocrine Tumors - drug therapy
/ Neuroendocrine Tumors - genetics
/ Neuroendocrine Tumors - pathology
/ Nuclear medicine
/ Octreotide
/ Octreotide - pharmacology
/ Penicillin
/ Rats
/ Reagents
/ Receptors
/ Receptors, Somatostatin - genetics
/ Regulatory mechanisms (biology)
/ Research and Analysis Methods
/ Somatostatin
/ Somatostatin receptors
/ Transcriptome - drug effects
/ Tumor cells
/ Tumors
/ Up-Regulation - drug effects
2020
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Elevated miR-16-5p induces somatostatin receptor 2 expression in neuroendocrine tumor cells
by
Lee, JongSook
, Yun, Mijin
, Jo, HanHee
, Kim, Taehun
, Pyun, Jae-Chul
, Lee, Misu
, Kwon, Hyeonjeong
, Kim, Jisu
, Park, Yusun
in
Analogs
/ Animals
/ Antineoplastic Agents, Hormonal - pharmacology
/ Apoptosis
/ Bioengineering
/ Biology and life sciences
/ Cancer
/ Care and treatment
/ Cell culture
/ Cell Line, Tumor
/ Cell proliferation
/ Development and progression
/ Gene expression
/ Gene Expression Regulation, Neoplastic - drug effects
/ Genetic aspects
/ Health aspects
/ HeLa Cells
/ Hormone receptors
/ Hormones
/ Humans
/ Laboratories
/ Life sciences
/ Materials science
/ Medicine and Health Sciences
/ MicroRNA
/ MicroRNAs
/ MicroRNAs - genetics
/ Neuroendocrine Cells - drug effects
/ Neuroendocrine Cells - metabolism
/ Neuroendocrine Cells - pathology
/ Neuroendocrine tumors
/ Neuroendocrine Tumors - drug therapy
/ Neuroendocrine Tumors - genetics
/ Neuroendocrine Tumors - pathology
/ Nuclear medicine
/ Octreotide
/ Octreotide - pharmacology
/ Penicillin
/ Rats
/ Reagents
/ Receptors
/ Receptors, Somatostatin - genetics
/ Regulatory mechanisms (biology)
/ Research and Analysis Methods
/ Somatostatin
/ Somatostatin receptors
/ Transcriptome - drug effects
/ Tumor cells
/ Tumors
/ Up-Regulation - drug effects
2020
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Elevated miR-16-5p induces somatostatin receptor 2 expression in neuroendocrine tumor cells
by
Lee, JongSook
, Yun, Mijin
, Jo, HanHee
, Kim, Taehun
, Pyun, Jae-Chul
, Lee, Misu
, Kwon, Hyeonjeong
, Kim, Jisu
, Park, Yusun
in
Analogs
/ Animals
/ Antineoplastic Agents, Hormonal - pharmacology
/ Apoptosis
/ Bioengineering
/ Biology and life sciences
/ Cancer
/ Care and treatment
/ Cell culture
/ Cell Line, Tumor
/ Cell proliferation
/ Development and progression
/ Gene expression
/ Gene Expression Regulation, Neoplastic - drug effects
/ Genetic aspects
/ Health aspects
/ HeLa Cells
/ Hormone receptors
/ Hormones
/ Humans
/ Laboratories
/ Life sciences
/ Materials science
/ Medicine and Health Sciences
/ MicroRNA
/ MicroRNAs
/ MicroRNAs - genetics
/ Neuroendocrine Cells - drug effects
/ Neuroendocrine Cells - metabolism
/ Neuroendocrine Cells - pathology
/ Neuroendocrine tumors
/ Neuroendocrine Tumors - drug therapy
/ Neuroendocrine Tumors - genetics
/ Neuroendocrine Tumors - pathology
/ Nuclear medicine
/ Octreotide
/ Octreotide - pharmacology
/ Penicillin
/ Rats
/ Reagents
/ Receptors
/ Receptors, Somatostatin - genetics
/ Regulatory mechanisms (biology)
/ Research and Analysis Methods
/ Somatostatin
/ Somatostatin receptors
/ Transcriptome - drug effects
/ Tumor cells
/ Tumors
/ Up-Regulation - drug effects
2020
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Elevated miR-16-5p induces somatostatin receptor 2 expression in neuroendocrine tumor cells
Journal Article
Elevated miR-16-5p induces somatostatin receptor 2 expression in neuroendocrine tumor cells
2020
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Overview
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.
Publisher
Public Library of Science,Public Library of Science (PLoS)
Subject
/ Animals
/ Antineoplastic Agents, Hormonal - pharmacology
/ Cancer
/ Gene Expression Regulation, Neoplastic - drug effects
/ Hormones
/ Humans
/ Medicine and Health Sciences
/ MicroRNA
/ Neuroendocrine Cells - drug effects
/ Neuroendocrine Cells - metabolism
/ Neuroendocrine Cells - pathology
/ Neuroendocrine Tumors - drug therapy
/ Neuroendocrine Tumors - genetics
/ Neuroendocrine Tumors - pathology
/ Rats
/ Reagents
/ Receptors, Somatostatin - genetics
/ Regulatory mechanisms (biology)
/ Research and Analysis Methods
/ Transcriptome - drug effects
/ Tumors
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