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Int. J. Mol. Sci. 2016, 17(4), 437;

Overexpression of TRPV3 Correlates with Tumor Progression in Non-Small Cell Lung Cancer

Department of Pathology, Harbin Medical University-Daqing, Daqing 163319, China
Department of Scientific Research, Third Affiliated Hospital of Guizhou Medical University, Duyun 558000, China
Department of Pharmacology, Harbin Medical University-Daqing, Daqing 163319, China
Department of Pathophysiology, Harbin Medical University-Daqing, Daqing 163319, China
Department of Pharmacology, Harbin Medical University, Harbin 150081, China
Department of Pathology, Daqing General Hospital Group Oilfield General Hospital, Daqing 163319, China
These authors contributed equally to this work.
Authors to whom correspondence should be addressed.
Academic Editor: William Chi-shing Cho
Received: 14 February 2016 / Revised: 11 March 2016 / Accepted: 11 March 2016 / Published: 24 March 2016
(This article belongs to the Collection Advances in Molecular Oncology)
Full-Text   |   PDF [3832 KB, uploaded 24 March 2016]   |  


(1) Background: Transient receptor potential vanilloid 3 (TRPV3) is a member of the TRP channels family of Ca2+-permeant channels. The proteins of some TRP channels are highly expressed in cancer cells. This study aimed to assess the clinical significance and biological functions of TRPV3 in non-small cell lung cancer (NSCLC); (2) Methods: Immunohistochemistry was used to detect the expression of TRPV3 in NSCLC tissues and adjacent noncancerous lung tissues. Western blot was used to detect the protein expressions of TRPV3, CaMKII, p-CaMKII, CyclinA, CyclinD, CyclinE1, CDK2, CDK4, and P27. Small interfering RNA was used to deplete TRPV3 expression. A laser scanning confocal microscope was used to measure intracellular calcium concentration ([Ca2+]i). Flow cytometry was used to analyze cell cycle; (3) Results: TRPV3 was overexpressed in 65 of 96 (67.7%) human lung cancer cases and correlated with differentiation (p = 0.001) and TNM stage (p = 0.004). Importantly, TRPV3 expression was associated with short overall survival. In addition, blocking or knockdown of TRPV3 could inhibit lung cancer cell proliferation. Moreover, TRPV3 inhibition could decrease [Ca2+]i of lung cancer cells and arrest cell cycle at the G1/S boundary. Further results revealed that TRPV3 inhibition decreased expressions of p-CaMKII, CyclinA, CyclinD1, CyclinE, and increased P27 level; (4) Conclusions: Our findings demonstrate that TRPV3 was overexpressed in NSCLC and correlated with lung cancer progression. TRPV3 activation could promote proliferation of lung cancer cells. TRPV3 might serve as a potential companion drug target in NSCLC. View Full-Text
Keywords: non-small cell lung cancer; TRPV3; proliferation; [Ca2+]i; cell cycle non-small cell lung cancer; TRPV3; proliferation; [Ca2+]i; cell cycle

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Li, X.; Zhang, Q.; Fan, K.; Li, B.; Li, H.; Qi, H.; Guo, J.; Cao, Y.; Sun, H. Overexpression of TRPV3 Correlates with Tumor Progression in Non-Small Cell Lung Cancer. Int. J. Mol. Sci. 2016, 17, 437.

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