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J Mol Endocrinol. 2015 Dec;55(3):183-96. doi: 10.1530/JME-15-0182. Epub 2015 Sep 4.

Modulatory role of miR-205 in angiogenesis and progression of thyroid cancer.

Author information

1
Cancer Molecular PathologySchool of Medicine, Griffith Medical School, Menzies Health Institute Queensland, Gold Coast Campus, Gold Coast, Queensland 4222, AustraliaFaculty of HealthInstitute of Health and Biomedical Innovation, Genomics Research Centre, Queensland University of Technology, Brisbane, Queensland, AustraliaPathology Queensland and Gold Coast University HospitalGold Coast, Queensland, Australia.
2
Cancer Molecular PathologySchool of Medicine, Griffith Medical School, Menzies Health Institute Queensland, Gold Coast Campus, Gold Coast, Queensland 4222, AustraliaFaculty of HealthInstitute of Health and Biomedical Innovation, Genomics Research Centre, Queensland University of Technology, Brisbane, Queensland, AustraliaPathology Queensland and Gold Coast University HospitalGold Coast, Queensland, Australia Cancer Molecular PathologySchool of Medicine, Griffith Medical School, Menzies Health Institute Queensland, Gold Coast Campus, Gold Coast, Queensland 4222, AustraliaFaculty of HealthInstitute of Health and Biomedical Innovation, Genomics Research Centre, Queensland University of Technology, Brisbane, Queensland, AustraliaPathology Queensland and Gold Coast University HospitalGold Coast, Queensland, Australia.
3
Cancer Molecular PathologySchool of Medicine, Griffith Medical School, Menzies Health Institute Queensland, Gold Coast Campus, Gold Coast, Queensland 4222, AustraliaFaculty of HealthInstitute of Health and Biomedical Innovation, Genomics Research Centre, Queensland University of Technology, Brisbane, Queensland, AustraliaPathology Queensland and Gold Coast University HospitalGold Coast, Queensland, Australia Cancer Molecular PathologySchool of Medicine, Griffith Medical School, Menzies Health Institute Queensland, Gold Coast Campus, Gold Coast, Queensland 4222, AustraliaFaculty of HealthInstitute of Health and Biomedical Innovation, Genomics Research Centre, Queensland University of Technology, Brisbane, Queensland, AustraliaPathology Queensland and Gold Coast University HospitalGold Coast, Queensland, Australia a.lam@griffith.edu.au.

Abstract

miR-205 plays a crucial role in angiogenesis and has been found in association with several types of cancers. The aims of this study were to investigate the clinical and functional roles of miR-205 on as the major initiator and modulator of angiogenesis in thyroid cancer. 101 thyroid carcinomas, including 51 conventional and 37 follicular variants of papillary thyroid carcinomas, and 13 undifferentiated thyroid carcinomas in addition to 13 lymph nodes with metastatic thyroid carcinoma were recruited to be compared with 14 nodular goitre and seven normal thyroid tissues. Five thyroid carcinoma cell lines, of papillary and undifferentiated origin with and without history of metastasis, were also used. Expression of vascular endothelial growth factor A (VEGFA) and miR-205 were measured and exogenous miR-205 were transfected to observe the changes of VEGFA (by immunofluorescence and western blot techniques). Proliferation assay, cell cycle analysis and apoptosis assays were also used to evaluate the role of miR-205 in these events. Significant under-expression of miR-205 and over-expression of VEGFA mRNA and protein were noticed in thyroid cancer tissues and cell lines compared to normal thyroid control. Transfection of miR-205 into the cancer cell lines caused significant reduction of VEGFA protein and significant inhibition in cell proliferation, arrest in G0-G1 of the cell cycle and promotion of total apoptosis (P<0.05). The angiogenic and tumour-suppressive roles of miRNA-205 were demonstrated for the first time in thyroid cancer. The current experiments provided specific information on the functional consequences of VEGF manipulation via miRNA on cancer.

KEYWORDS:

Papillary thyroid carcinoma; Undifferentiated thyroid carcinoma; VEGF; miR-205; microRNA

PMID:
26342107
DOI:
10.1530/JME-15-0182
[Indexed for MEDLINE]

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