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β-Cryptoxanthin Reduced Lung Tumor Multiplicity and Inhibited Lung Cancer Cell Motility by Downregulating Nicotinic Acetylcholine Receptor α7 Signaling
Cancer prevention research (Philadelphia, Pa.), 2016-11, Vol.9 (11), p.875-886
Iskandar, Anita R
Miao, Benchun
Li, Xinli
Hu, Kang-Quan
Liu, Chun
Wang, Xiang-Dong
2016
Volltextzugriff (PDF)
Details
Autor(en) / Beteiligte
Iskandar, Anita R
Miao, Benchun
Li, Xinli
Hu, Kang-Quan
Liu, Chun
Wang, Xiang-Dong
Titel
β-Cryptoxanthin Reduced Lung Tumor Multiplicity and Inhibited Lung Cancer Cell Motility by Downregulating Nicotinic Acetylcholine Receptor α7 Signaling
Ist Teil von
Cancer prevention research (Philadelphia, Pa.), 2016-11, Vol.9 (11), p.875-886
Ort / Verlag
United States
Erscheinungsjahr
2016
Quelle
MEDLINE
Beschreibungen/Notizen
Despite the consistent association between a higher intake of the provitamin A carotenoid β-cryptoxanthin (BCX) and a lower risk of lung cancer among smokers, potential mechanisms supporting BCX as a chemopreventive agent are needed. We first examined the effects of BCX on 4-[methyl nitrosamino]-1-[3-pyridyl]-1-butanone (NNK)-induced lung tumorigenesis in A/J mice. BCX supplementation was given daily to the mice starting 2 weeks prior to the injection of NNK and continued 16 weeks after NNK injection. BCX supplementation resulted in a dose-dependent increase of BCX concentration in both serum and lungs of the mice without a significant alteration of vitamin A (retinol and retinyl palmitate) concentration. BCX significantly reduced the multiplicity of the NNK-induced lung tumor by 52% to 63% compared with the NNK-treated mice without BCX supplementation. The protective effect of BCX in the lungs was associated with reductions of both mRNA and protein of the homopentameric neuronal nicotinic acetylcholine receptor α7 (α7-nAChR), which has been implicated in lung tumorigenesis. We then conducted an in vitro cell culture study and found that BCX treatment suppressed α7-nAChR expression and inhibited the migration and invasion of α7-nAChR-positive lung cancer cells but not in cells lacking α7-nAChR. The activities of BCX were significantly attenuated by activators of α7-nAChR/PI3K signaling or by overexpression of constitutively active PI3K. Collectively, the results suggest that BCX inhibits lung tumorigenesis and cancer cell motility through the downregulation of α7-nAChR/PI3K signaling, independent of its provitamin A activity. Therefore, BCX can be used as a chemopreventive agent or a chemotherapeutic compound against lung cancer. Cancer Prev Res; 9(11); 875-86. ©2016 AACR.
Sprache
Englisch
Identifikatoren
ISSN: 1940-6207
eISSN: 1940-6215
DOI: 10.1158/1940-6207.CAPR-16-0161
Titel-ID: cdi_proquest_miscellaneous_1835506123
Format
–
Schlagworte
alpha7 Nicotinic Acetylcholine Receptor - metabolism
,
Animals
,
Antineoplastic Agents - pharmacology
,
Beta-Cryptoxanthin - pharmacology
,
Cell Line, Tumor
,
Cell Movement - drug effects
,
Down-Regulation
,
Humans
,
Lung Neoplasms - pathology
,
Mice
,
Signal Transduction - drug effects
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