annonacin and Breast-Neoplasms

annonacin has been researched along with Breast-Neoplasms* in 1 studies

Other Studies

1 other study(ies) available for annonacin and Breast-Neoplasms

Article	Year
Annonacin induces cell cycle-dependent growth arrest and apoptosis in estrogen receptor-α-related pathways in MCF-7 cells. Journal of ethnopharmacology, 2011, Oct-11, Volume: 137, Issue:3 Tamoxifen resistance is common in estrogen receptor-α (ERα)-positive breast cancers. Pawpaw and soursop are anticancer annonaceous plants in complementary medicine. Thus, we studied the effects of annonacin, an annonaceous acetogenin, in breast cancer cells.. Cell growth and ERα-related pathways were studied. The effects of annonacin were tested in MCF-7 xenografts in nude mice.. In ERα-positive MCF-7 cells, annonacin (half-effective dose ED(50) = 0.31 μM) and 4-hydroxytamoxifen (ED(50) = 1.13 μM) decreased cell survival whereas annonacin (0.5-1 μM) increased cell death at 48 h. Annonacin and 4-hydroxytamoxifen were additive in inhibiting cell survival. Annonacin (0.1 μM) induced G(0)/G(1) growth arrest while increasing p21(WAF1) and p27(kip1) and decreasing cyclin D1 protein expression. Annonacin (0.1μM) decreased cyclin D1 protein expression more than 4-hydroxytamoxifen (1 μM). Annonacin (0.1 μM) increased apoptosis while decreasing Bcl-2 protein expression. The combination of annonacin (0.1 μM) and 4-hydroxytamoxifen (1 μM) decreased Bcl-2 protein expression and ERα transcriptional activity more than annonacin (0.1 μM) did alone. Annonacin, but not 4-hydroxytamoxifen, decreased ERα protein expression. Moreover, annonacin decreased phosphorylation of ERK1/2, JNK and STAT3. In nude mice, annonacin decreased MCF-7 xenograft tumor size at 7-22 days. Moreover, annonacin decreased ERα, cyclin D1 and Bcl-2 protein expression in the xenograft at 22 days.. Annonacin induced growth arrest and apoptosis in ERα-related pathways in MCF-7 cells. Annonacin and 4-hydroxytamoxifen were additive in inhibiting cell survival and ERα transcriptional activity. Moreover, annonacin attenuated MCF-7 xenograft tumor growth while inhibiting ERα, cyclin D1 and Bcl-2 protein expressions in nude mice. Topics: Animals; Antineoplastic Agents, Phytogenic; Apoptosis; Breast Neoplasms; Cell Cycle Checkpoints; Cell Line, Tumor; Cyclin D1; Cyclin-Dependent Kinase Inhibitor p21; Cyclin-Dependent Kinase Inhibitor p27; Dose-Response Relationship, Drug; Estrogen Antagonists; Estrogen Receptor alpha; Extracellular Signal-Regulated MAP Kinases; Female; Furans; Humans; JNK Mitogen-Activated Protein Kinases; Lactones; Mice; Mice, Inbred BALB C; Mice, Nude; Phosphorylation; Proto-Oncogene Proteins c-bcl-2; Signal Transduction; STAT3 Transcription Factor; Tamoxifen; Time Factors; Transfection; Tumor Burden; Xenograft Model Antitumor Assays	2011

Article

Year

Annonacin induces cell cycle-dependent growth arrest and apoptosis in estrogen receptor-α-related pathways in MCF-7 cells.

Journal of ethnopharmacology, 2011, Oct-11, Volume: 137, Issue:3

Tamoxifen resistance is common in estrogen receptor-α (ERα)-positive breast cancers. Pawpaw and soursop are anticancer annonaceous plants in complementary medicine. Thus, we studied the effects of annonacin, an annonaceous acetogenin, in breast cancer cells.. Cell growth and ERα-related pathways were studied. The effects of annonacin were tested in MCF-7 xenografts in nude mice.. In ERα-positive MCF-7 cells, annonacin (half-effective dose ED(50) = 0.31 μM) and 4-hydroxytamoxifen (ED(50) = 1.13 μM) decreased cell survival whereas annonacin (0.5-1 μM) increased cell death at 48 h. Annonacin and 4-hydroxytamoxifen were additive in inhibiting cell survival. Annonacin (0.1 μM) induced G(0)/G(1) growth arrest while increasing p21(WAF1) and p27(kip1) and decreasing cyclin D1 protein expression. Annonacin (0.1μM) decreased cyclin D1 protein expression more than 4-hydroxytamoxifen (1 μM). Annonacin (0.1 μM) increased apoptosis while decreasing Bcl-2 protein expression. The combination of annonacin (0.1 μM) and 4-hydroxytamoxifen (1 μM) decreased Bcl-2 protein expression and ERα transcriptional activity more than annonacin (0.1 μM) did alone. Annonacin, but not 4-hydroxytamoxifen, decreased ERα protein expression. Moreover, annonacin decreased phosphorylation of ERK1/2, JNK and STAT3. In nude mice, annonacin decreased MCF-7 xenograft tumor size at 7-22 days. Moreover, annonacin decreased ERα, cyclin D1 and Bcl-2 protein expression in the xenograft at 22 days.. Annonacin induced growth arrest and apoptosis in ERα-related pathways in MCF-7 cells. Annonacin and 4-hydroxytamoxifen were additive in inhibiting cell survival and ERα transcriptional activity. Moreover, annonacin attenuated MCF-7 xenograft tumor growth while inhibiting ERα, cyclin D1 and Bcl-2 protein expressions in nude mice.

Topics: Animals; Antineoplastic Agents, Phytogenic; Apoptosis; Breast Neoplasms; Cell Cycle Checkpoints; Cell Line, Tumor; Cyclin D1; Cyclin-Dependent Kinase Inhibitor p21; Cyclin-Dependent Kinase Inhibitor p27; Dose-Response Relationship, Drug; Estrogen Antagonists; Estrogen Receptor alpha; Extracellular Signal-Regulated MAP Kinases; Female; Furans; Humans; JNK Mitogen-Activated Protein Kinases; Lactones; Mice; Mice, Inbred BALB C; Mice, Nude; Phosphorylation; Proto-Oncogene Proteins c-bcl-2; Signal Transduction; STAT3 Transcription Factor; Tamoxifen; Time Factors; Transfection; Tumor Burden; Xenograft Model Antitumor Assays

2011