Abstract
Large-scale epidemiological cohort studies performed in the United States indicate that breast cancer risk is associated with active and passive smoking. As of yet, however, there is no direct evidence of antitumor effects by agents that block the effect of tobacco compound nicotine (Nie) on relevant nicotinic receptors (nAChR) involved in breast tumorigenesis. In the present study, the expression profiles of different nAChR subunits in the human breast cancer cell line (MDA-MB-231) were characterized by RT-PCR. Nic (>0.1 μ, 6 h) significantly increased α9-nAChR mRNA and protein expression levels in human breast cancer cells (MDA-MB-231 cells). On the other hand, combined treatment with luteolin (Lut, 0.5 μ and quercetin (Que, 0.5 μ.M) profoundly decreased MDA-MB-231 proliferation by down-regulating α9-nAChR expression. MDA-MB-231 cells were cultured in soft agar to evaluate anchorage-independent colony formation; combined treatment of Lut + Que inhibited Nic-induced MDA-MB-231 colony formation. Interestingly, the number of colonies formed was profoundly reduced in α9-nAChR knockdown (Si α9) cells in the combined (Lut + Que)-treated group as compared to the relevant control groups. Such results show that Lut- or Que-induced antitransforming activities were not limited to specific inhibition of the α9-nAChR receptor. Both α5- and α9-nAChR appear to be important molecular targets for Lut- and Que-induced antitumor effects in human breast cancer cells.
| Original language | English |
|---|---|
| Pages (from-to) | 235-241 |
| Number of pages | 7 |
| Journal | Journal of Agricultural and Food Chemistry |
| Volume | 58 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - Jan 13 2010 |
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Keywords
- Breast cancer
- Luteolin
- Nicotinic receptor
- Quercetin
ASJC Scopus subject areas
- Agricultural and Biological Sciences(all)
- Chemistry(all)
Cite this
Combination treatment with luteolin and quercetin enhances antiproliferative effects in nicotine-treated MDA-MB-231 cells by down-regulating nicotinic acetylcholine receptors. / Shih, Yung Leun; Liu, Hui Ching; Chen, Ching Shyang; Hsu, Chung-Huei; Pan, Min Hsiung; Chang, Hui Wen; Chang, Chien Hsi; Chen, Feng Chia; Ho, Chi Tang; Yang, Yi-Yuan; Ho, Yuan-Soon.
In: Journal of Agricultural and Food Chemistry, Vol. 58, No. 1, 13.01.2010, p. 235-241.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Combination treatment with luteolin and quercetin enhances antiproliferative effects in nicotine-treated MDA-MB-231 cells by down-regulating nicotinic acetylcholine receptors
AU - Shih, Yung Leun
AU - Liu, Hui Ching
AU - Chen, Ching Shyang
AU - Hsu, Chung-Huei
AU - Pan, Min Hsiung
AU - Chang, Hui Wen
AU - Chang, Chien Hsi
AU - Chen, Feng Chia
AU - Ho, Chi Tang
AU - Yang, Yi-Yuan
AU - Ho, Yuan-Soon
PY - 2010/1/13
Y1 - 2010/1/13
N2 - Large-scale epidemiological cohort studies performed in the United States indicate that breast cancer risk is associated with active and passive smoking. As of yet, however, there is no direct evidence of antitumor effects by agents that block the effect of tobacco compound nicotine (Nie) on relevant nicotinic receptors (nAChR) involved in breast tumorigenesis. In the present study, the expression profiles of different nAChR subunits in the human breast cancer cell line (MDA-MB-231) were characterized by RT-PCR. Nic (>0.1 μ, 6 h) significantly increased α9-nAChR mRNA and protein expression levels in human breast cancer cells (MDA-MB-231 cells). On the other hand, combined treatment with luteolin (Lut, 0.5 μ and quercetin (Que, 0.5 μ.M) profoundly decreased MDA-MB-231 proliferation by down-regulating α9-nAChR expression. MDA-MB-231 cells were cultured in soft agar to evaluate anchorage-independent colony formation; combined treatment of Lut + Que inhibited Nic-induced MDA-MB-231 colony formation. Interestingly, the number of colonies formed was profoundly reduced in α9-nAChR knockdown (Si α9) cells in the combined (Lut + Que)-treated group as compared to the relevant control groups. Such results show that Lut- or Que-induced antitransforming activities were not limited to specific inhibition of the α9-nAChR receptor. Both α5- and α9-nAChR appear to be important molecular targets for Lut- and Que-induced antitumor effects in human breast cancer cells.
AB - Large-scale epidemiological cohort studies performed in the United States indicate that breast cancer risk is associated with active and passive smoking. As of yet, however, there is no direct evidence of antitumor effects by agents that block the effect of tobacco compound nicotine (Nie) on relevant nicotinic receptors (nAChR) involved in breast tumorigenesis. In the present study, the expression profiles of different nAChR subunits in the human breast cancer cell line (MDA-MB-231) were characterized by RT-PCR. Nic (>0.1 μ, 6 h) significantly increased α9-nAChR mRNA and protein expression levels in human breast cancer cells (MDA-MB-231 cells). On the other hand, combined treatment with luteolin (Lut, 0.5 μ and quercetin (Que, 0.5 μ.M) profoundly decreased MDA-MB-231 proliferation by down-regulating α9-nAChR expression. MDA-MB-231 cells were cultured in soft agar to evaluate anchorage-independent colony formation; combined treatment of Lut + Que inhibited Nic-induced MDA-MB-231 colony formation. Interestingly, the number of colonies formed was profoundly reduced in α9-nAChR knockdown (Si α9) cells in the combined (Lut + Que)-treated group as compared to the relevant control groups. Such results show that Lut- or Que-induced antitransforming activities were not limited to specific inhibition of the α9-nAChR receptor. Both α5- and α9-nAChR appear to be important molecular targets for Lut- and Que-induced antitumor effects in human breast cancer cells.
KW - Breast cancer
KW - Luteolin
KW - Nicotinic receptor
KW - Quercetin
UR - http://www.scopus.com/inward/record.url?scp=75249101732&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=75249101732&partnerID=8YFLogxK
U2 - 10.1021/jf9031684
DO - 10.1021/jf9031684
M3 - Article
C2 - 19921817
AN - SCOPUS:75249101732
VL - 58
SP - 235
EP - 241
JO - Journal of Agricultural and Food Chemistry
JF - Journal of Agricultural and Food Chemistry
SN - 0021-8561
IS - 1
ER -