Antiproliferation and apoptosis induced by tamoxifen in human bile duct carcinoma QBC939 cells via upregulated p53 expression

Peng, Han; Kang, Jinhe; Li, Hualiang; Hu, Shaojun; Lian, Hui-Hui; Qiu, Pingping; Zhang, Jian; Li, Wengang; Chen, Qing‐Xi

doi:10.1016/j.bbrc.2009.05.059

Cited by 24 publications

(22 citation statements)

References 16 publications

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“…One mechanism of action is by TAM inducing apoptotic cell death, demonstrated in many cell types including breast cancer. 1–3 In this malignancy, adjuvant radiation and chemotherapies are effective because they induce tumor cell death 4,5 and resistance to adjuvant therapies may arise when treatment does not cause apoptosis. Therefore it is important to understand the mechanisms involved to enhance cell death.…”

Section: Introductionmentioning

confidence: 99%

Tamoxifen regulates cell fate through mitochondrial estrogen receptor beta in breast cancer

et al. 2012

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Tamoxifen has both cytostatic and cytotoxic properties for breast cancer. Tamoxifen engaged mitochondrial estrogen receptor beta (ERβ) as an antagonist in MCF-7 BK cells, increasing reactive oxygen species (ROS) concentrations from the mitochondria that were required for cytotoxicity. In part this derived from tamoxifen down-regulating manganese superoxide dismutase (MnSOD) activity through nitrosylating tyrosine 34, thereby increasing ROS. ROS activated protein kinase C delta and c-jun N-terminal kinases, resulting in the mitochondrial translocation of Bax and cytochrome C release. Interestingly, tamoxifen failed to cause high ROS levels or induce cell death in MCF7BK-TR cells due to stimulation of MnSOD activity through agonistic effects at mitochondrial ERβ. In several mouse xenograft models, lentiviral shRNA-induced knockdown of MnSOD caused tumors that grew in the presence of tamoxifen to undergo substantial apoptosis. Tumor MnSOD and mitochondrial ERβ are therefore targets for therapeutic intervention to reverse tamoxifen resistance and enhance a cell death response.

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Section: Introductionmentioning

confidence: 99%

Tamoxifen regulates cell fate through mitochondrial estrogen receptor beta in breast cancer

et al. 2012

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“…After 4 h incubation at 37 o C, the medium was removed and 100 ȝl DMSO was added to each well. The optical absorbance (A) of each well was then read at 490 nm [5] . The percentage of viable cells was calculated as follows: (A of experimental group/A of control group) ×100%.…”

Section: Cell Viability Assaymentioning

confidence: 99%

“…BrieÀy, cells growing logarithmically were grown to of 5×10 4 cells/ well and transfected with siRNA in a 96-well plate for 24 or 48 h [5] . At the end of the transfected, media containing were removed and 200 ȝl MTT (5 mg/ml in PBS, St. Louis, MO, USA) was added in each well.…”

Section: Cell Viability Assaymentioning

confidence: 99%

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Study on the Effect of ER-alpha 36 siRNA on the Growth of ER Negative Breast Cancer Cells

Zhang

Gao

Li³

et al. 2012

2012 International Conference on Biomedical Engineering and Biotechnology

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Objective: To investigate the effect of ER-Į36 siRNA on the growth of ER -breast cancer cell. Methods: The inhibitive effects of ER-Į36 siRNA with various concentration on ER negative breast cancer cell at 24 h and 48 h were determined with MTT, the changes in DNA quantity was detected by Annexin V-FITC/PI staining, the expression levels of ER-Į36 and pro-caspase-3 by Western blot. Results: ER-Į36 siRNA could inhibited the growth of ER -breast cancer cells lines in vitro. The apoptosis rates at early phase treated with ER-Į36 siRNA were 15.5%. The expression of ER-Į36 decreased significantly after ER-Į36 siRNA treatment. Conclusions: ER-Į36 siRNA could induced the apoptosis in ER-Į36 dependent manner and had specificity to induce apoptosis of ER negative breast cancer cells.

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“…Tamoxifen is a selective estrogen receptor modulator that is widely used as the adjuvant therapy for breast cancer. It produces therapeutic efficacy in breast cancer by binding to the estrogen receptor, by inhibiting protein kinase C activity (30) or by up-regulating p53 expression (31). In addition, tamoxifen exhibits P-glycoprotein-reversing (32) and BCRP-reversing activities (33), suggesting that it may potentially be capable of killing the cancer stem cells.…”

Section: Introductionmentioning

confidence: 99%

Effects of stealth liposomal daunorubicin plus tamoxifen on the breast cancer and cancer stem cells

Guo

Zhou

Xue³

et al. 2010

J Pharm Pharm Sci

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-Purpose: The cancer stem cells play an important role in the invasion, metastasis and relapse of cancers as they are resistant to regular chemotherapy. In the present study, stealth liposomal daunorubicin plus tamoxifen was developed for eradicating breast cancer cells together with cancer stem cells. Methods: Inhibitory effects were performed on the bulk human breast cancer cells (MCF-7), the sorted MCF-7 cancer stem-like cells (side population, SP), and the sorted MCF-7 cancer cells (NSP), respectively. Antitumor activity and TUNEL analysis were evaluated on the MCF-7 xenografts in nude mice. Results: The encapsulation efficiencies of daunorubicin and tamoxifen were 95% and 90%, respectively. The mean particle size of the stealth liposomes was about 100 nm. Breast cancer stem cells were identified by the specific markers CD44+/CD24-, and isolated from bulk MCF-7 cells. When applying stealth liposomal daunorubicin plus tamoxifen, the inhibitory effects on both the breast cancer cells and the cancer stem cells were significantly increased in vitro, respectively. In the MCF-7 xenografts in mice, stealth liposomal daunorubicin plus tamoxifen showed the most favorable antitumor activity due to the passive targeting the tumor tissue and the synergistic effects in eliminating breast cancer cells and cancer stem cells. Conclusions: Stealth liposomal daunorubicin plus tamoxifen could have the potentials in eliminating both breast cancer cells and cancer stem cells. _______________________________________________________________________________________

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Antiproliferation and apoptosis induced by tamoxifen in human bile duct carcinoma QBC939 cells via upregulated p53 expression

Cited by 24 publications

References 16 publications

Tamoxifen regulates cell fate through mitochondrial estrogen receptor beta in breast cancer

Tamoxifen regulates cell fate through mitochondrial estrogen receptor beta in breast cancer

Study on the Effect of ER-alpha 36 siRNA on the Growth of ER Negative Breast Cancer Cells

Effects of stealth liposomal daunorubicin plus tamoxifen on the breast cancer and cancer stem cells

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