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Recent findings of an inverse association between β-cryptoxanthin and lung cancer risk in several observational epidemiologic studies suggest that β-cryptoxanthin could potentially act as a chemopreventive agent against lung cancer. However, the biological activity of β-cryptoxanthin and molecular mechanism(s) by which β-cryptoxanthin affects lung tumourigenesis have not been studied. In the present study, we found that β-cryptoxanthin inhibited the growth of A549 cells, a non-small-cell lung cancer cell line and BEAS-2B cells, an immortalized human bronchial epithelial cell line in a dose-dependent manner. β-Cryptoxanthin suppressed the protein levels of cyclin D1 and cyclin E, up-regulated the cell cycle inhibitor p21, increased the number of lung cancer cells in theG1/G0 phase and decreased those in the S phase of the cell cycle. Consistent with inhibition of the lung cancer cell growth, β-cryptoxanthin induced the mRNA levels of retinoic acid receptor β (RARβ) in BEAS-2B cells, although this effect was less pronounced in A549 cells. Furthermore, β-cryptoxanthin transactivated RAR-mediated transcription activity of the retinoic acid response element. These findings suggest a mechanism of anti-proliferative action of β-cryptoxanthin and indicate that β-cryptoxanthin may be a promising chemopreventive agent against lung cancer.