Abstract
Sulforaphane (SFN), a natural compound derived from broccoli/broccoli sprouts, has been demonstrated to be used as an antitumor agent in different types of cancers. However, its antitumor effect in thyroid cancer remains largely unknown. The aim of the study was to investigate the therapeutic potential of SFN for thyroid cancer and explore the mechanisms underlying antitumor effects of SFN by in vitro and in vivo studies. 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. Mechanically, SFN inhibited thyroid cancer cell growth and invasiveness through repressing phosphorylation of Akt, enhancing p21 expression by the activation of Erk and p38 signaling cascades, and promoting mitochondrial-mediated apoptosis via reactive oxygen species (ROS)-dependent pathway. Growth of xenograft tumors derived from thyroid cancer cell line FTC133 in nude mice was also significantly inhibited by SFN. Importantly, we did not find significant effect of SFN on body weight and liver function of mice. Collectively, we for the first time demonstrate that SFN is a potentially effective antitumor agent for thyroid cancer.
Highlights
Thyroid cancer is a common endocrine malignancy that has rapidly increased in global incidence in the past 15 years [1, 2]
Primary thyroid cancer is classified into three major histopathologic types [3]: differentiated thyroid cancers (DTCs), including papillary (PTC, 85% of cases) and follicular (FTC, 5%–10%); medullary thyroid cancer (MTC, 5%); anaplastic thyroid cancer (ATC, 1%)
SFN, a dietary isothiocyanate found in broccoli and cauliflower, has been widely used for treatment of inflammatory diseases and recent studies have indicated its antitumor effects in cell lines and animals [14, 15, 20, 21]
Summary
Thyroid cancer is a common endocrine malignancy that has rapidly increased in global incidence in the past 15 years [1, 2]. Recent advances in understanding the molecular pathogenesis of thyroid cancer have shown great promise to develop more effective treatment for thyroid cancer [3]. This has mainly resulted from the identification of molecular alterations in major signaling pathways, such as the RAS/RAF/MEK/MAPK/ERK (MAPK) and PI3K/Akt pathways, which play critical roles in cell transformation, survival and metastasis, and become classical therapeutical targets for thyroid cancer [3, 5, 6]. In addition to targeted therapies, in recent years, some of natural product-derived drugs display potent antitumor activity in thyroid cancer, such as paclitaxel, vincristine, vinorelbine and shikonin [7,8,9,10]
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