CENPF promotes papillary thyroid cancer progression by mediating cell proliferation and apoptosis.

Papillary thyroid cancer (PTHCA) accounts for ~85% cases of thyroid cancer and exhibits high incidence. Targeted therapy is an effective method to combat this disease; however, novel therapeutic targets are required. Centromere protein F (CENPF), a member of centromere proteins and a transient kinetochore protein, regulates various cellular processes such as cell migration and mitosis, and its upregulation has been observed in multiple types of cancer, including breast cancer and gastric cancer. However, the potential role of CENPF in PTHCA progression is remains unclear. The results of the current study demonstrated that CENPF expression was enhanced in human PTHCA tissues through IHC assays. Furthermore, the expression of CENPF was correlated with the prognosis and the clinicopathological features, including T stage (P=0.021) and intraglandular dissemination (P=0.042) in patients with PTHCA. CENPF regulated the proliferation, apoptosis and cell cycle of PTHCA cells in vitro, which was confirmed through colony formation, MTT and flow cytometry assays, and affected tumor growth in vivo in mice. In conclusion, the current study reported the involvement of CENPF in PTHCA progression and provided a promising therapeutic target for PTHCA treatment.

miR-137 suppresses the invasion and procedure of EMT of human breast cancer cell line MCF-7 through targeting CtBP1.

Distant metastasis is the predominant site of gastric cancer recurrence and the most common cause of death. Recently, accumulating evidence has established that aberrant epithelial-mesenchymal transition activation plays a crucial role in the genesis, invasion, and metastasis of various cancers, including breast cancer. In this paper, we found that miR-137, which has been reported to function as a tumor suppressor in a variety of cancers, could significantly suppress the migration and invasion of MCF-7 cells, which might be correlated with its suppressive effects on the EMT procedure. Upon transfection, the epithelial marker, E-cadherin, was up-regulated, and the mesenchymal markers, N-cadherin and Vimentin, were suppressed. Moreover, we also found that carboxyl-terminal binding protein 1 (CtBP1) was a putative target gene of miR-137 in MCF-7 cells, and might be involved in the suppressive effects, which might provide novel diagnostic and therapeutic options for human breast cancer in the future.