MicroRNA-1280 modulates cell growth and invasion of thyroid carcinoma through targeting estrogen receptor α
Corresponding Author(s) : D Meng
Cellular and Molecular Biology,
Vol. 62 No. 3: Issue 3
Abstract
Thyroid cancer (TC) is one of the most common endocrine malignancies, with a steadily increasing incidence and lethality over the last several decades. ERα is a nuclear hormone receptor that has a key role in different cellular process and participates in the development and progression of thyroid cancer. ERα is the predicted target gene of microRNA-1280 (miR-1280). The present study was designed to delineate the role and underlying mechanism of miR-1280 in regulating thyroid cancer through targeting ERα. In our study, we analyzed the expression level of miR-1280 in thyroid cancer and detected significantly lower miR-1280 levels in TC tissue and cell lines compared with adjacent normal tissue or healthy cell line. We then overexpressed miR-1280 by miRNA mimic transfection and inhibited miR-1280 by miRNA inhibitor transfection. The inhibition of miR-1280 significantly elevated proliferation and invasion ability, whereas overexpression of miR-1280 inhibited cell growth and invasion in TC cells. Additionally, the luciferase reporter assay confirmed a targeting reaction between miR-1280 and ERα. Furthermore, overexpression of miR-1280 inhibited ERα and ERK pathway expression in TC cells, indicating that miR-1280 acts as a tumor suppressor by inhibiting the expression of ERα. Taken together, we demonstrated that overexpressed miR-1280 levels in TC cells may promote cell proliferation and invasion by inhibiting ERα, which might provide a new therapeutic target for thyroid cancer.
Keywords
Thyroid cancer
ERα
miR-1280
ERK pathway.
Meng, D., Li, Z., Ma, X., Fu, L., & Qin, G. (2016). MicroRNA-1280 modulates cell growth and invasion of thyroid carcinoma through targeting estrogen receptor α. Cellular and Molecular Biology, 62(3), 1–6. Retrieved from https://www.cellmolbiol.org/index.php/CMB/article/view/811
Download Citation
Endnote/Zotero/Mendeley (RIS)BibTeX