Cell cycle protein cyclin Y is associated with human non-small-cell lung cancer proliferation and tumorigenesis

The role of cell cycle protein cyclin Y (CCNY) in non-small-cell lung cancer (NSCLC) is not clear. Hence, the aim of this study was to explore the potential role of CCNY in lung cancer.

Real-time quantitative polymerase chain reaction was used for detecting the expression of CCNY mRNA in 60 samples from patients with NSCLC. The functional role of CCNY in NSCLC cells was evaluated by small interfering RNA-mediated depletion of the protein followed by analysis of cell proliferation, anchorage-independent growth, and xenograft growth.

CCNY mRNA is overexpressed (N = 60) in samples from patients with NSCLC. Furthermore, CCNY mRNA expression positively correlated with histologic types (squamous cell carcinoma vs. adenocarcinomas; P = .048) and with the tumor size (size > 3 cm vs. size ≤ 3 cm; P = .010) in NSCLC. Functionally, CCNY depletion was shown to inhibit cell proliferation and anchorage-independent growth in lung cancer cells. Moreover, the proliferation effects were increased when CCNY was overexpressed in lung cancer cells. Finally, CCNY was shown to support H1299 and 95D xenograft growth in nude mice.

We reported for the first time (to the best of our knowledge) that CCNY was overexpressed in samples of NSCLC. CCNY mRNA expression associated with histologic types of NSCLC and promoted the malignant growth of lung cancer cell line in vivo and in vitro. Thus, these results validated the role of CCNY as a clinically relevant human oncoprotein and warrant further investigation of CCNY as a biomarker and a therapeutic target in NSCLC.