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Disease Markers
Volume 2017, Article ID 6136401, 8 pages
Research Article

CACNA1B (Cav2.2) Overexpression and Its Association with Clinicopathologic Characteristics and Unfavorable Prognosis in Non-Small Cell Lung Cancer

1Department of Respiratory Medicine, The First Affiliated Hospital of Soochow University, Suzhou, China
2Department of Respiratory Medicine, Affiliated Hospital of Nantong University, Nantong, Jiangsu 226001, China
3Department of Pathology, Affiliated Hospital of Nantong University, Nantong, Jiangsu 226001, China
4Department of Laboratory Medicine, Affiliated Hospital of Nantong University, Nantong, Jiangsu 226001, China

Correspondence should be addressed to Jianan Huang; moc.621@tnnanaijgnauh

Received 13 July 2016; Revised 5 September 2016; Accepted 8 September 2016; Published 3 January 2017

Academic Editor: Stamatios E. Theocharis

Copyright © 2017 Xiaoyu Zhou et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


CACNA1B (2.2) encodes an N-type voltage-gated calcium channel (VGCC) ubiquitously expressed in brain and peripheral nervous system that is important for regulating neuropathic pain. Because intracellular calcium concentration is a key player in cell proliferation and apoptosis, VGCCs are implicated in tumorigenesis. Recent studies have identified CACNA1B (2.2) being overexpressed in prostate and breast cancer tissues when compared to adjacent normal tissues; however, its role in non-small cell lung cancer (NSCLC) has not been investigated. In this study, we determined the mRNA and protein expression of CACNA1B (2.2) in NSCLC tumorous and adjacent nontumorous tissues by quantitative reverse transcription PCR (qRT-PCR) and tissue microarray immunohistochemistry analysis (TMA-IHC), respectively. CACNA1B (2.2) protein expressions in tumorous tissues were correlated with NSCLC patients’ clinical characteristics and overall survival. CACNA1B (2.2) mRNA and protein expression levels were higher in NSCLC tumorous tissues than in nontumorous tissues. High CACNA1B (2.2) protein expression was associated with higher TNM stages, and CACNA1B (2.2) protein expression is an independent prognostic marker in NSCLC. Based on our results, we conclude that CACNA1B (2.2) plays a role in NSCLC development and progression. Elucidating the underlying mechanism may help design novel treatment by specifically targeting the calcium regulation pathway for NSCLC, a devastating disease with increasing incidence and mortality in China.