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Int. J. Mol. Sci. 2016, 17(4), 437; doi:10.3390/ijms17040437

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

1
Department of Pathology, Harbin Medical University-Daqing, Daqing 163319, China
2
Department of Scientific Research, Third Affiliated Hospital of Guizhou Medical University, Duyun 558000, China
3
Department of Pharmacology, Harbin Medical University-Daqing, Daqing 163319, China
4
Department of Pathophysiology, Harbin Medical University-Daqing, Daqing 163319, China
5
Department of Pharmacology, Harbin Medical University, Harbin 150081, China
6
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)
View Full-Text   |   Download PDF [3832 KB, uploaded 24 March 2016]   |  

Abstract

(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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