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.

MicroRNA-205 suppresses the invasion and epithelial-mesenchymal transition of human gastric cancer cells.

Distant metastasis is the predominant pattern of gastric cancer (GC) recurrence, and is the most common cause of cancer­associated mortality. Accumulating evidence has suggested that aberrant activation of epithelial­mesenchymal transition has a crucial role in the genesis, invasion and metastasis of various types of cancer, including GC. Using Cell Counting kit­8 and Transwell assays, the effects of microRNA (miR)­205 on the proliferation, migration and invasion of NCI­H87 GC cells were determined, and the potential underlying mechanisms were explored. The results of the present study demonstrated that miR­205, which has been reported to function as a tumor suppressor in various types of cancer, significantly suppressed the migration and invasion of GC cells, which may be correlated with its suppressive effects on EMT. Upon transfection with miR­205, the epithelial marker CDH1 (E­cadherin) was upregulated, and the mesenchymal markers CDH2 (N­cadherin) and vimentin were suppressed. Furthermore, zinc­finger E­box­binding homeobox factor­1 (ZEB1) was identified as a putative target gene of miR­205 in GC, which may be associated with its suppressive effects. The results of the present study may provide novel diagnostic and therapeutic options for the treatment of human GC.

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.

miR-137 impairs the proliferative and migratory capacity of human non-small cell lung cancer cells by targeting paxillin.

Human lung cancer is the leading cause of cancer motility worldwide, with nearly 1.4 million deaths each year, among which non-small cell lung cancer (NSCLC) accounts for almost 85% of this disease. The discovery of microRNAs (miRNAs) provides a new avenue for NSCLC diagnostic and treatment regiments. Currently, a large number of miRNAs have been reported to be associated with the progression of NSCLC, among which serum miR-137 has been examined to be down-regulated in NSCLC patients. However, the function of miR-137 on NSCLC cells migration and invasion and the relative mechanisms were less known. Here, we found that ectopic expression of miR-137 could inhibit cell proliferation, induce cell apoptosis, and suppress cell migration and invasion in NSCLC cell line A549. Moreover, we found that paxillin (PXN) was a target gene of miR-137 in NSCLC cells and restored expression of PXN abolished the miR-137-mediated suppression of cell migration and invasion. Taken together, our results showed that miR-137 acted as a tumor suppressor in NSCLC by targeting PXN, and it may provide novel diagnostic and therapeutic options for human NSCLC clinical operation in future.