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ARS Home » Northeast Area » Boston, Massachusetts » Jean Mayer Human Nutrition Research Center On Aging » Research » Publications at this Location » Publication #204053
Title: Beta-Cryptoxanthin Suppresses the Growth of Immortalized Human Bronchial Epithelial Cells

Author
item LIAN, FUZHI - HNRCA AT TUFTS
item HU, KANG-QUAN - HNRCA AT TUFTS
item Russell, Robert
item Wang, Xiang-Dong

Submitted to: International Journal of Cancer
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/9/2006
Publication Date: 11/1/2006
Citation: Lian, F., Hu, K., Russell, R., Wang, X. 2006. Beta-Cryptoxanthin Suppresses the Growth of Immortalized Human Bronchial Epithelial Cells. International Journal of Cancer. 119(3): 2084-2089.

Interpretive Summary: Recent epidemiological studies have suggested the preventive effect of beta-cryptoxanthin, a carotenoid rich in orange and orange juice, against lung cancer. However, the biological activity of beta-cryptoxanthin and molecular mechanism(s) by which beta-cryptoxanthin affects lung tumorigenesis have not been studied. In the present study, we found that beta-cryptoxanthin inhibited the growth of pre-cancer and cancer cells derived from lung tissue, suppressed the expression of cyclin D1 and cyclin E cell growth regulators, up-regulated the cell growth inhibitor p21, thereby blocked cell cycle progression. Consistent with inhibition of the lung cancer cell growth, beta-cryptoxanthin induced the expression of retinoic acid receptor beta (RAR-beta) tumor suppressor gene, which was associated with the activation of vitamin A-mediated signaling pathway. These findings suggest a mechanism of anti-cancer activity of beta-cryptoxanthin and indicate that beta-cryptoxanthin may be a promising chemopreventive agent against lung cancer.

Technical Abstract: Recent findings of an inverse association between beta-cryptoxanthin and lung cancer risk in several observational epidemiologic studies suggests that beta-cryptoxanthin could potentially act as a chemopreventive agent against lung cancer. However, the biological activity of beta-cryptoxanthin and molecular mechanism(s) by which beta-cryptoxanthin affects lung tumorigenesis has not been studied. In the present study, we found that beta-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. Beta-cryptoxanthin suppressed the protein levels of cyclin D1 and cyclin E, up-regulated the cell cycle inhibitor p21, increased the number of lunch cancer cells in the G1/G0 phase and decreased those in the S phase of the cell cycle. Consistent with inhibition of the lung cancer cell growth, beta-cryptoxanthin induced the mRNA levels of retinoic acid receptor Beta (RAR-beta) in BEAS-2B cells, although this effect was less pronounced in A549 cells. Furthermore, beta-cryptoxanthin transactivated the RAR-mediated transcription activity of the retinoic acid response element (RARE). These findings suggest a mechanism of anti-proliferative action of beta-cryptoxanthin and indicate that beta-cryptoxanthin may be a promising chemopreventive agent against lunch cancer.