Cell Cycle Kinetic Effects of Tamoxifen on Human Breast Cancer Cells

Danova, Marco; Pellicciari, C.; Zibera, C.; Mangiarotti, Rosanna; Gibelli, N.; Giordano, Monica; Wang, Eugenia; Mazzini, Giuliano; Riccardi, Alberto

doi:10.1111/j.1749-6632.1993.tb17206.x

Cited by 14 publications

(2 citation statements)

References 6 publications

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“…By contrast, treatment with TAM or NDAM did not induce a significantly greater G 0 /G 1 -phase arrests in the MCF-7 cells compared with TAM/NDAM cotreatment. Previous studies have shown that TAM induces significant G 0 /G 1 -phase arrest in breast cancer cells ( 20 , 22 ). Furthermore, in agreement with the present study, Li et al ( 23 ) showed that combined treatment of TAM with organoselenium compounds enhanced apoptosis.…”

Section: Discussionmentioning

confidence: 95%

“…When NDAM was combined with a subapoptotic dose of the chemotherapeutic agent, significant apoptosis was induced. The primary growth inhibitory mechanism for TAM in MCF-7 cells has been reported to be cell cycle inhibition ( 20 , 21 ). In the present study, TAM/NDAM treatment was found to induce significant G 0 /G 1 -phase arrest in the MCF-7 cells.…”

Section: Discussionmentioning

confidence: 99%

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Nordamnacanthal potentiates the cytotoxic effects of tamoxifen in human breast cancer cells

Subramani

Yeap

et al. 2014

Oncology Letters

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Tamoxifen (TAM) is the mainline drug treatment for breast cancer, despite its side effects and the development of resistance. As an alternative approach, in the present study a novel combination therapy was established through combining TAM with nordamnacanthal (NDAM) in order to investigate the additive effect of these drugs in MCF-7 human breast cancer cells. A significant dose-dependent reduction in cell viability and an increase in apoptosis were observed in the MCF-7 cells cotreated with TAM and NDAM compared with the untreated control cells or the cells treated with TAM and NDAM alone (P<0.05). The cytotoxic influence of the combination of TAM and NDAM was found to be two-fold that of the individual agents. Annexin V/propidium iodide double-staining revealed the typical nuclear features of apoptosis. Furthermore, an increase in the proportion of apoptotic, Annexin V-positive cells was observed with the combination therapy. Moreover, this apoptotic induction was associated with a collapse of the mitochondrial membrane potential and the generation of reactive oxygen species. To the best of our knowledge, the findings of the present study are the first to suggest that combining TAM with NDAM may be a potential combination therapy for the treatment of breast cancer and may have the potential to minimize or eliminate the side effects associated with high doses of TAM.

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Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 99%

Nordamnacanthal potentiates the cytotoxic effects of tamoxifen in human breast cancer cells

Subramani

Yeap

et al. 2014

Oncology Letters

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Endocrine response and resistance in breast cancer: a role for the transcription factor Fos

Gee¹,

Willsher²,

Kenny³

et al. 1999

Int. J. Cancer

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We have previously demonstrated that elevated Fos expression may be important in de novo endocrine resistance in breast cancer. However, changes in Fos expression during endocrine response and subsequently on acquisition of resistance are unknown. This study immunocytochemically monitors Fos protein within sequential biopsies from primary human breast cancer patients obtained pre‐treatment (T1), during tamoxifen therapy (T2, T3) and on disease progression (T5), examining in parallel proliferation [i.e., MIB1 (Ki67) immunostaining, mitotic activity], cellularity and endocrine response. Significantly diminished Fos, proliferation and cellularity were observed after 6 weeks of therapy in patients exhibiting a better quality and/or duration of response, while modest Fos increases and a maintained proliferation and cellularity were seen in poorer responders. Decreases in Fos, proliferation and cellularity at 6 months similarly hallmarked better responders. We confirmed a significant association between de novo resistance and elevated Fos and proliferation. Additionally, however, these parameters increased at the time of disease relapse over pre‐treatment and “on therapy” values. Our data indicate that tamoxifen response involves a reduction in both tumor cell proliferation and cell survival, potentially entailing diminished Fos protein expression in better‐responding patients. Our data are also supportive of elevated Fos expression being involved in the departure from endocrine control inherent in both primary and acquired resistance. Int. J. Cancer (Pred. Oncol.) 84:54–61, 1999. © 1999 Wiley‐Liss, Inc.

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