MicroRNA 483-3p targets Pard3 to potentiate TGF-β1-induced cell migration, invasion, and epithelial-mesenchymal transition in anaplastic thyroid cancer cells

Oncogene
Xiaoping ZhangZhongwei Lv

Abstract

Anaplastic thyroid cancer (ATC) is associated with poor prognosis and is often untreatable. MicroRNA 483-3p (miR-483) and partitioning-defective 3 (Pard3), a member of the Pard family, have functions and regulatory mechanisms in ATC. The abnormal regulation of miR-483 may play an important role in tumorigenesis, and Par3 is known to regulate cell polarity, cell migration, and cell division. Tumor proliferation promoted by the regulation of miRNA expression can be regulated in thyroid cancer by upregulating transforming growth factor-β1 (TGF-β1), which is thought to interact with Pard3. When compared with adjacent non-tumor tissues, we found that miR-483 was upregulated and Pard3 was downregulated in 80 thyroid tumor samples. Disease-free survival was decreased when expression of miR-483 was upregulated and Pard3 expression was downregulated. Cell growth, migration, and invasion were induced by overexpression of miR-483. However, knockdown of miR-483 resulted in a loss of cell invasion and viability, both in vitro and in vivo. The expression of Pard3 was increased by the inhibition of miR-483, but TGF-β1-induced cell migration and invasion were decreased by miR-483 inhibition. A dual-luciferase reporter assay determined that Par...Continue Reading

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Jun 9, 2019·Cells·Cinzia AntognelliVincenzo N Talesa
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Jun 9, 2021·Oncogene·Farzaneh Atashrazm, Sarah Ellis

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Methods Mentioned

BETA
nucleotide exchange
transfection
PCR
Assay
electrophoresis
pull
GTPase
pull down
xenograft

Software Mentioned

tile
SPSS

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