Combination treatment with luteolin and quercetin enhances antiproliferative effects in nicotine-treated MDA-MB-231 cells by down-regulating nicotinic acetylcholine receptors

Yung Leun Shih, Hui Ching Liu, Ching Shyang Chen, Chung-Huei Hsu, Min Hsiung Pan, Hui Wen Chang, Chien Hsi Chang, Feng Chia Chen, Chi Tang Ho, Yi-Yuan Yang, Yuan-Soon Ho

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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 languageEnglish
Pages (from-to)235-241
Number of pages7
JournalJournal of Agricultural and Food Chemistry
Volume58
Issue number1
DOIs
Publication statusPublished - Jan 13 2010

Fingerprint

Luteolin
cholinergic receptors
nicotine
luteolin
Quercetin
Nicotinic Receptors
Nicotine
breast neoplasms
quercetin
Cells
Breast Neoplasms
Tobacco
cells
Tobacco Smoke Pollution
receptors
Agar
cohort studies
Antineoplastic Agents
carcinogenesis
breasts

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 journalArticle

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. / Combination treatment with luteolin and quercetin enhances antiproliferative effects in nicotine-treated MDA-MB-231 cells by down-regulating nicotinic acetylcholine receptors. In: Journal of Agricultural and Food Chemistry. 2010 ; Vol. 58, No. 1. pp. 235-241.
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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.",
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T1 - Combination treatment with luteolin and quercetin enhances antiproliferative effects in nicotine-treated MDA-MB-231 cells by down-regulating nicotinic acetylcholine receptors

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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

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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.

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