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Inhibition of NF-kappaB-mediated transcription and induction of apoptosis in human breast cancer cells by epoxypseudoisoeugenol-2-methyl butyrate.
Cancer Chemother Pharmacol. 2009 Mar; 63(4):673-80.CC

Abstract

PURPOSE

Breast cancer is one of the most prevalent woman cancers. Genomic instability, accumulative mutations, and subsequent changes in intracellular signaling cascades play key roles in the development of human breast cancers. Activation of nuclear factor-kappaB (NF-kappaB) has been implicated in oncogenesis of breast cancers and is known to be associated with resistance to anticancer agents and apoptosis. Blocking NF-kappaB signaling may represent a therapeutic strategy in breast cancer therapy. The objective of this study is to investigate the in vitro effects of epoxypseudoisoeugenol-2-methyl butyrate (EPB), a phenylpropranoid isolated from Pimpinella corymbosa, on the activation of NF-kappaB, cell growth, cell cycle progression and apoptosis in MCF-7 (estrogen-dependent) and BT-549 (estrogen-independent) breast cancer cells.

METHODS

Transcriptional activity of NF-kappaB was measured by cell based reporter gene assay. Cell proliferation was determined by MTT assay. Cell cycle analysis was carried out by flow cytometry and apoptosis was observed by DAPI staining assy.

RESULTS

EPB inhibited the NF-kappaB-mediated transcription activity induced by tumor necrosis factor-alpha (TNF-alpha) and phorbol myristate acetate (PMA) in MCF-7 cells. EPB also inhibited constitutive NF-kappaB transcriptional activity in BT-549 cells. EPB inhibited the proliferation of both MCF-7 and BT-549 cells in a concentration- and time-dependent manner. EPB induced cell cycle arrest in G(1)/G(0) phase and apoptosis in both MCF-7 and BT 549 cells.

CONCLUSIONS

These in vitro results indicated that EPB has a potential for use against both hormone-dependent and hormone-independent breast cancers and its effects seem to be mediated by inhibiting the NF-kappaB activity.

Authors+Show Affiliations

National Center for Natural Products Research, Research Institute of Pharmaceutical Sciences, The University of Mississippi, Mississippi 38677, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, Non-P.H.S.

Language

eng

PubMed ID

18597088

Citation

Ma, Guoyi, et al. "Inhibition of NF-kappaB-mediated Transcription and Induction of Apoptosis in Human Breast Cancer Cells By Epoxypseudoisoeugenol-2-methyl Butyrate." Cancer Chemotherapy and Pharmacology, vol. 63, no. 4, 2009, pp. 673-80.
Ma G, Tabanca N, Husnu Can Baser K, et al. Inhibition of NF-kappaB-mediated transcription and induction of apoptosis in human breast cancer cells by epoxypseudoisoeugenol-2-methyl butyrate. Cancer Chemother Pharmacol. 2009;63(4):673-80.
Ma, G., Tabanca, N., Husnu Can Baser, K., Kirimer, N., Pasco, D. S., Khan, I. A., & Khan, S. I. (2009). Inhibition of NF-kappaB-mediated transcription and induction of apoptosis in human breast cancer cells by epoxypseudoisoeugenol-2-methyl butyrate. Cancer Chemotherapy and Pharmacology, 63(4), 673-80. https://doi.org/10.1007/s00280-008-0784-9
Ma G, et al. Inhibition of NF-kappaB-mediated Transcription and Induction of Apoptosis in Human Breast Cancer Cells By Epoxypseudoisoeugenol-2-methyl Butyrate. Cancer Chemother Pharmacol. 2009;63(4):673-80. PubMed PMID: 18597088.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Inhibition of NF-kappaB-mediated transcription and induction of apoptosis in human breast cancer cells by epoxypseudoisoeugenol-2-methyl butyrate. AU - Ma,Guoyi, AU - Tabanca,Nurhayat, AU - Husnu Can Baser,K, AU - Kirimer,Nese, AU - Pasco,David S, AU - Khan,Ikhlas A, AU - Khan,Shabana I, Y1 - 2008/07/03/ PY - 2008/02/10/received PY - 2008/06/05/accepted PY - 2008/7/4/pubmed PY - 2009/4/1/medline PY - 2008/7/4/entrez SP - 673 EP - 80 JF - Cancer chemotherapy and pharmacology JO - Cancer Chemother Pharmacol VL - 63 IS - 4 N2 - PURPOSE: Breast cancer is one of the most prevalent woman cancers. Genomic instability, accumulative mutations, and subsequent changes in intracellular signaling cascades play key roles in the development of human breast cancers. Activation of nuclear factor-kappaB (NF-kappaB) has been implicated in oncogenesis of breast cancers and is known to be associated with resistance to anticancer agents and apoptosis. Blocking NF-kappaB signaling may represent a therapeutic strategy in breast cancer therapy. The objective of this study is to investigate the in vitro effects of epoxypseudoisoeugenol-2-methyl butyrate (EPB), a phenylpropranoid isolated from Pimpinella corymbosa, on the activation of NF-kappaB, cell growth, cell cycle progression and apoptosis in MCF-7 (estrogen-dependent) and BT-549 (estrogen-independent) breast cancer cells. METHODS: Transcriptional activity of NF-kappaB was measured by cell based reporter gene assay. Cell proliferation was determined by MTT assay. Cell cycle analysis was carried out by flow cytometry and apoptosis was observed by DAPI staining assy. RESULTS: EPB inhibited the NF-kappaB-mediated transcription activity induced by tumor necrosis factor-alpha (TNF-alpha) and phorbol myristate acetate (PMA) in MCF-7 cells. EPB also inhibited constitutive NF-kappaB transcriptional activity in BT-549 cells. EPB inhibited the proliferation of both MCF-7 and BT-549 cells in a concentration- and time-dependent manner. EPB induced cell cycle arrest in G(1)/G(0) phase and apoptosis in both MCF-7 and BT 549 cells. CONCLUSIONS: These in vitro results indicated that EPB has a potential for use against both hormone-dependent and hormone-independent breast cancers and its effects seem to be mediated by inhibiting the NF-kappaB activity. SN - 1432-0843 UR - https://www.unboundmedicine.com/medline/citation/18597088/Inhibition_of_NF_kappaB_mediated_transcription_and_induction_of_apoptosis_in_human_breast_cancer_cells_by_epoxypseudoisoeugenol_2_methyl_butyrate_ DB - PRIME DP - Unbound Medicine ER -