J Nutr Biochem. 2015 Feb 14. pii: S0955-2863(15)00028-5. doi: 10.1016/j.jnutbio.2014.12.012. [Epub ahead of print]
Alpha-carotene inhibits metastasis in Lewis lung carcinoma in vitro, and suppresses lung metastasis and tumor growth in combination with taxol in tumor xenografted C57BL/6 mice.
Abstract
This
study aimed to investigate the anti-metastatic activity of α-carotene
(AC) in Lewis lung carcinoma (LLC) and in combination with taxol in
LLC-xenografted C57BL/6 mice. Cell culture studies reveal that AC
significantly inhibited invasion, migration and activities of matrix
metalloproteinase (MMP)-2, -9 and urokinase plasminogen activator but
increased protein expression of tissue inhibitor of MMP (TIMP)-1, -2 and
plasminogen activator inhibitor (PAI)-1.
These effects of AC are similar to those of β-carotene at the same concentration (2.5μM). AC (2.5μM) also significantly inhibited integrin β1-mediated phosphorylation of focal adhesion kinase (FAK) which then decreased the phosphorylation of MAPK family. Findings from the animal model reveal that AC treatment (5mg/kg) alone significantly decreased lung metastasis without affecting primary tumor growth, whereas taxol treatment (6mg/kg) alone exhibited significant inhibition on both actions, as compared to tumor control group.
AC treatment alone significantly decreased protein expression of integrin β1 but increased protein expression of TIMP-1 and PAI-1 without affecting protein expression of TIMP-2 and phosphorylation of FAK in lung tissues, whereas taxol treatment alone significantly increased protein expression of TIMP-1, PAI-1 and TIMP-2 but decreased protein expression of integrin β1 and phosphorylation of FAK.
The combined treatment produced stronger actions on lung metastasis and lung tissues protein expression of TIMP-1, TIMP-2 and PAI-1. Overall, we demonstrate that AC effectively inhibits LLC metastasis and suppresses lung metastasis in combination with taxol in LLC-bearing mice, suggesting that AC could be used as an anti-metastatic agent or as an adjuvant for anti-cancer drugs.
Copyright © 2015. Published by Elsevier Inc.
These effects of AC are similar to those of β-carotene at the same concentration (2.5μM). AC (2.5μM) also significantly inhibited integrin β1-mediated phosphorylation of focal adhesion kinase (FAK) which then decreased the phosphorylation of MAPK family. Findings from the animal model reveal that AC treatment (5mg/kg) alone significantly decreased lung metastasis without affecting primary tumor growth, whereas taxol treatment (6mg/kg) alone exhibited significant inhibition on both actions, as compared to tumor control group.
AC treatment alone significantly decreased protein expression of integrin β1 but increased protein expression of TIMP-1 and PAI-1 without affecting protein expression of TIMP-2 and phosphorylation of FAK in lung tissues, whereas taxol treatment alone significantly increased protein expression of TIMP-1, PAI-1 and TIMP-2 but decreased protein expression of integrin β1 and phosphorylation of FAK.
The combined treatment produced stronger actions on lung metastasis and lung tissues protein expression of TIMP-1, TIMP-2 and PAI-1. Overall, we demonstrate that AC effectively inhibits LLC metastasis and suppresses lung metastasis in combination with taxol in LLC-bearing mice, suggesting that AC could be used as an anti-metastatic agent or as an adjuvant for anti-cancer drugs.
Copyright © 2015. Published by Elsevier Inc.
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