Effects of combined treatment with rapamycin and cotylenin A, a novel differentiation-inducing agent, on human breast carcinoma MCF-7 cells and xenografts

Kasukabe, Takashi; Okabe‐Kado, Junko; Kato, Nobuo; Sassa, Takeshi; Honma, Yoshio

doi:10.1186/bcr1344

Cited by 57 publications

(59 citation statements)

References 32 publications

(52 reference statements)

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“…For example, fusicoccin A shows antitumor activity [52], promotes platelet aggregation [53] and stabilizes the inhibitory binding of 14-3-3 to ERa [54]. Cotylenin A has been shown to induce differentiation in myeloid leukemia [55], display activity against breast cancer cells [56] and stabilize the inhibitory binding of 14-3-3 proteins to c-Raf [57,58]. We have furthermore shown that a semisynthetic derivative of fusicoccin -FC-THF -enhances transport of the potassium channel TASK3 to the plasma membrane by stabilizing 14-3-3 binding to the C terminus of TASK3 [59].…”

Section: Forskolinmentioning

confidence: 99%

Stabilization of protein–protein interactions by small molecules

Giordanetto¹,

Schäfer

Ottmann

2014

Drug Discovery Today

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Section: Forskolinmentioning

confidence: 99%

Stabilization of protein–protein interactions by small molecules

Giordanetto¹,

Schäfer

Ottmann

2014

Drug Discovery Today

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“…The in vivo experiments were performed in accordance with the guidelines of our institute. For mice in MCF7 xenograft study, the mice were given injections of β-estradiol (Sigma) dissolved in pure sesame oil (0.1 mg per 0.05 ml sesame oil per mouse, subcutaneously) 1 day before the injection of MCF7 cells and then at weekly intervals [30,31]. Mice were inoculated subcutaneously with 2 × 10 7 MCF7 cells.…”

Section: Antitumor Activity Of Pdtc In Tumor Xenograft Modelmentioning

confidence: 99%

NF-κB pathway inhibitors preferentially inhibit breast cancer stem-like cells

Zhou

Zhang

et al. 2007

Breast Cancer Res Treat

197

157

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Accumulating evidence indicates that breast cancer is caused by cancer stem cells and cure of breast cancer requires eradication of breast cancer stem cells. Previous studies with leukemia stem cells have shown that NF-κB pathway is important for leukemia stem cell survival. In this study, by using MCF7 sphere cells as model of breast cancer stem-like cells, we evaluated the effect of NF-κB pathway specific inhibitors on human breast cancer MCF7 sphere cells. Three inhibitors including parthenolide (PTL), pyrrolidinedithiocarbamate (PDTC) and its analog diethyldithiocarbamate (DETC) were found to preferentially inhibit MCF7 sphere cell proliferation. These compounds also showed preferential inhibition in term of proliferation and colony formation on MCF7 side population (SP) cells, a small fraction of MCF7 cells known to enrich in breast cancer stem-like cells. The preferential inhibition effect of these compounds was due to inhibition of the NF-κB activity in both MCF7 sphere and MCF7 cells, with higher inhibition effect on MCF7 sphere cells than on MCF7 cells. PDTC was further evaluated in vivo and showed significant tumor growth inhibition alone but had better tumor growth inhibition in combination with paclitaxel in the mouse xenograft model than either PDTC or paclitaxel alone. This study suggests that breast cancer stem-like cells could be selectively inhibited by targeting signaling pathways important for breast cancer stem-like cells.

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“…In accordance with the literature (20) regarding the establishment of MCF-7 human breast xenografts, mice were administered exogenous estrogen (10 mg/kg) twice a week by intraperitoneal injection for 2 weeks. MCF-7 cells (5x10 6 ) in 100 μl D-Hank's were subsequently injected s.c. into the right flank of each mouse.…”

Section: Growth Inhibitory Effects Measured By Mtt Colorimetrymentioning

confidence: 99%

Chemically modified siRNA directed against the KDR gene inhibits the proliferation of breast cancer cells

Zhang¹,

Zhang²,

Hou³

et al. 2008

Mol Med Rep

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Abstract. Vascular endothelial growth factor receptor-2 or kinase insert domain-containing receptor (VEGFR2/KDR) is secreted by most solid tumors, including breast cancer, and is an important mediator of angiogenesis. To observe the effects of KDR gene expression on cell proliferation and the cell cycle in MCF-7 cells in vitro and in vivo, we used chemically modified siRNA directed against KDR. The results revealed that chemically modified siRNA transfection of the KDR gene effectively inhibited the proliferation of MCF-7 cells, arrested cells in the G1 phase and down-regulated the expression of KDR. In addition, in the progression of cell cycle arrest induced by siRNA, phosphorylated ERK and CDK1 expression was down-regulated (P<0.01). In vivo, the growth of tumors was visibly suppressed. RT-PCR and the results of immunohistochemistry indicated that KDR mRNA and protein expression was reduced in the excised tumors. In contrast, there were no obvious changes in the control groups. This implies that chemically modified KDR siRNA markedly decreases KDR gene expression and inhibits cellular proliferation in vitro, as well as suppressing tumor growth in a xenograft model. KDR may be a new target for breast cancer treatment. IntroductionAngiogenesis is a complex process that is essential for tumor growth beyond 1 or 2 mm 3 . Kinase insert domain-containing receptor (KDR), commonly known as VEGFR2, is one of the best characterized pro-angiogenic factors, playing a critical role in physiological and pathological angiogenesis (1). Via its interaction with VEGF, KDR mediates many key components of angiogenesis, including endothelial cell proliferation, invasion, migration and survival, as well as vessel permeability.It also plays an important role in the regulation of tumor genesis and development (2-4). In addition to activating KDR on vessels in a paracrine manner, VEGF secreted by tumor cells also activates KDR on itself in an autocrine manner, and directly promotes the growth of tumor cells (5-10). Therefore, by inhibiting the expression of KDR, tumor growth can be suppressed on two levels.With one million new cases presenting each year, breast cancer is the most common cancer among women and the leading cause of death worldwide in those between the ages of 30 and 70 years (11,12). In human breast cancer, levels of KDR have been correlated with tumor progression and invasion (13). KDR and VEGF are co-expressed in primary breast carcinomas, and their expression is increased when tumors shift to an angiogenic phenotype (14,15). Many investigators are beginning to advocate silencing the gene expression of angiogenic factors as an anti-angiogenic strategy.RNA interference (RNAi ) is a novel gene therapy technology (16,17) in which 21-25 nucleotide small interfering RNA (siRNA) duplexes, homologous to the silenced gene, function as sequence-specific RNAi mediators, suppressing the expression of the target gene. siRNA synthesis in vitro is the latest development in RNAi; however, the poor stability and specificity of siRNA...

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Effects of combined treatment with rapamycin and cotylenin A, a novel differentiation-inducing agent, on human breast carcinoma MCF-7 cells and xenografts

Cited by 57 publications

References 32 publications

Stabilization of protein–protein interactions by small molecules

Stabilization of protein–protein interactions by small molecules

NF-κB pathway inhibitors preferentially inhibit breast cancer stem-like cells

Chemically modified siRNA directed against the KDR gene inhibits the proliferation of breast cancer cells

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