TY - JOUR
T1 - Pterostilbene Inhibits Adipocyte Conditioned-Medium-Induced Colorectal Cancer Cell Migration through Targeting FABP5-Related Signaling Pathway
AU - Hsiao, Yu Hsuan
AU - Chen, Nien Chi
AU - Koh, Yen Chun
AU - Nagabhushanam, Kalyanam
AU - Ho, Chi Tang
AU - Pan, Min Hsiung
N1 - Funding Information:
This study was supported by the Ministry of Science and Technology [105-2320-B-002-031-MY3, 105-2628-B-002-003-MY3, 107-2321-B-002-050].
Publisher Copyright:
© 2019 American Chemical Society.
PY - 2019/9/18
Y1 - 2019/9/18
N2 - Pterostilbene (PTS) is a phenolic compound with diverse pharmacologic activities. However, its potential for inhibiting obesity-related colorectal cancer (CRC) remains unclear. Our study evaluated the mechanism of inhibitory effects of PTS on adipocyte conditioned-medium (aCM)-induced malignant transformation in HT-29 colorectal adenocarcinoma cells. The results demonstrated that PTS could downregulate the expression of aCM-induced fatty acid-binding protein 5 (FABP5) and prometastatic factors such as vascular endothelial growth factor, matrix metalloproteinase-2 (MMP2), MMP9, and extracellular tumor necrosis factor α via inhibiting aCM-induced nuclear factor-kappa B (NF-κB), β-catenin, and peroxisome proliferator-activated receptor γ(PPAR-γ). Moreover, PTS can suppress aCM-stimulated phosphoinositide 3-kinase (PI3K), protein kinase B (Akt), p38 mitogen-activated protein kinase (p38 MAPK), extracellular signal-regulated kinase (ERK), and c-Jun N-terminal kinases 1/2 (JNK 1/2) signaling pathways activation that are upstream of NF-κB, β-catenin, and PPAR-γ. Therefore, we suggest that PTS could alleviate adiposity-induced metastasis in CRC via inhibiting cell migration through downregulating FABP5 gene expression.
AB - Pterostilbene (PTS) is a phenolic compound with diverse pharmacologic activities. However, its potential for inhibiting obesity-related colorectal cancer (CRC) remains unclear. Our study evaluated the mechanism of inhibitory effects of PTS on adipocyte conditioned-medium (aCM)-induced malignant transformation in HT-29 colorectal adenocarcinoma cells. The results demonstrated that PTS could downregulate the expression of aCM-induced fatty acid-binding protein 5 (FABP5) and prometastatic factors such as vascular endothelial growth factor, matrix metalloproteinase-2 (MMP2), MMP9, and extracellular tumor necrosis factor α via inhibiting aCM-induced nuclear factor-kappa B (NF-κB), β-catenin, and peroxisome proliferator-activated receptor γ(PPAR-γ). Moreover, PTS can suppress aCM-stimulated phosphoinositide 3-kinase (PI3K), protein kinase B (Akt), p38 mitogen-activated protein kinase (p38 MAPK), extracellular signal-regulated kinase (ERK), and c-Jun N-terminal kinases 1/2 (JNK 1/2) signaling pathways activation that are upstream of NF-κB, β-catenin, and PPAR-γ. Therefore, we suggest that PTS could alleviate adiposity-induced metastasis in CRC via inhibiting cell migration through downregulating FABP5 gene expression.
KW - adipocyte conditioned-medium (aCM)
KW - colorectal cancer (CRC)
KW - fatty acid-binding protein 5 (FABP5)
KW - obesity
KW - pterostilbene (PTS)
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U2 - 10.1021/acs.jafc.9b03997
DO - 10.1021/acs.jafc.9b03997
M3 - Article
C2 - 31419115
AN - SCOPUS:85072353316
SN - 0021-8561
VL - 67
SP - 10321
EP - 10329
JO - Journal of Agricultural and Food Chemistry
JF - Journal of Agricultural and Food Chemistry
IS - 37
ER -