Abstract LB-B22: CCNY2 promotes lung cancer cell migration and invasion via regulating F-actin expression

Abstract

Abstract Background: Cyclin Y (CCNY) is a novel cyclin and is highly conserved in metazoan species. Cyclin Y mRNA has several transcripts and only ccny1 and ccny2 has been documented. A potential CDK partner of Cyclin Y is PFTAIRE kinase (PFTK1). In hepatocellular carcinoma, cell motility and invasion was enhanced by PFTK1 expression. But the function of CCNY1 and CCNY2 on cell migration and invasiveness has not been reported yet. Methods: Recombined plasmids carrying CCNY1 and CCNY2 were constructed and transfected to H1299 cells to obtain CCNY up-regulation cells. A lentivirus-based RNAi delivery system was used to inhibit CCNY mRNA expression. The role of CCNY in cell motility and invasion was investigated using wound healing and transwell assay. The protein levels in lung cancer cells were determined by western-blot, immunofluorescence technique and high-content cell analysis. Mouse xenograft experiments were carried out to study the metastasis ability of CCNY1 and CCNY2 in vivo. Immunohistochemistry was used to detect the CCNY protein level of lung cancer tissues. Results: cell motility and invasion activity were inhibited and MET (Mesenchymal - Epithelial Transition) was caused by down-regulating of CCNY in 95D and H1299 cells. CCNY2 could enhance cell migration and invasion activity in vivo and vitro. The F-actin level was regulated by CCNY2 expression. In non-small cell lung cancer tissues, CCNY2 was highly expressed and the CCNY2 expression was associated with histological grade. Conclusion: CCNY2 was firstly detected in lung cancer cells and non-small cell lung cancer tissues. Our findings demonstrated CCNY2 not CCNY1 promoted cell motility and invasion by regulating the expression of F-actin and modulating intracellular cytoskeletal components. Citation Format: xiaoting zhao, Mei Jiang, wentao Yue. CCNY2 promotes lung cancer cell migration and invasion via regulating F-actin expression. [abstract]. In: Proceedings of the AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; 2015 Nov 5-9; Boston, MA. Philadelphia (PA): AACR; Mol Cancer Ther 2015;14(12 Suppl 2):Abstract nr LB-B22.