The aim of this study is to identify its expression, function, and molecular mechanism in thyroid cancer. microRNA-137 (miR-137) downregulation was observed in thyroid cancer tissues compared with normal thyroid tissues. miR-137 mimics downregulated B-CPAP cell proliferation, colony formation ability, and invasion, with suppressed expression of cyclin E, MMP2, p-ERK, and p-AKT. miR-137 inhibitor transfection in TPC-1 cell line showed the opposite effects.
Our data demonstrated that SFN significantly inhibited thyroid cancer cell proliferation in a dose- and time-dependent manner, induced G2/M phase cell cycle arrest and apoptosis, and inhibited thyroid cancer cell migration and invasion by suppressing epithelial-mesenchymal transition (EMT) process and expression of Slug, Twist, MMP-2 and -9.
Our data also showed that shikonin dramatically inhibited thyroid cancer cell migration and invasion by suppressing epithelial-mesenchymal transition and downregulating expression of Slug and MMP-2, -9, and -14.
In addition to its apoptotic effect, phenylbutyrate (PB), a carboxylic acid HDACI, inhibited an anaplastic (ATC) thyroid cancer cell line ARO from penetrating a matrigel coated transwell with concomitant suppression of a metastasis-associated gene, matrix metalloproteinase-7 (MMP-7) and stimulation of a transformation suppressor protein, reversion-inducing- cysteine-rich protein with Kazal motifs without affecting MMP-2 expression levels.