Roles of the Bcl-2/Bax Ratio, Caspase-8 and 9 in Resistance of Breast Cancer Cells to Paclitaxel

Sharifi, Simin; Barar, Jaleh; Hejazi, Mohammad Saeid; Samadi, Nasser

doi:10.7314/apjcp.2014.15.20.8617

Cited by 89 publications

(63 citation statements)

References 54 publications

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“…Bcl-2 and Bax are 2 important mitochondria-mediated caspase-dependent apoptotic proteins. It has been proven that Bax forms a complex with the anti-apoptotic protein Bcl-2 to balance its apoptotic effects (15). The ratio of Bcl-2/Bax was used to determine whether cells undergo programmed cell death.…”

Section: Resultsmentioning

confidence: 99%

Induction of apoptosis in nasal polyp-derived fibroblasts by bleomycin A5 inï¿½vitro

Tian

et al. 2018

Mol Med Report

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The present study aimed to evaluate the pro-apoptotic effects of bleomycin A5 on nasal polyp‑derived fibroblasts (NPDFs) and the underlying molecular mechanisms. Nasal polyp tissue was acquired from 10 patients during surgery and NPDFs were isolated from surgical tissues. Fibroblasts were identified using immunohistochemistry. Bleomycin A5 was used to treat NPDFs along a concentration gradient. Cell viability was evaluated using a Cell Counting Kit‑8 assay. A flow cytometric Annexin V‑fluorescein isothiocyanate/propidium iodide assay was used to determine the percentage of apoptotic NPDFs. The mRNA expression levels of apoptotic genes were determined by reverse transcription‑quantitative polymerase chain reaction and levels of proteins associated with apoptosis were determined by western blotting. The results indicated that bleomycin A5 was able to induce apoptosis in NPDFs in a dose‑dependent manner. NPDFs treated with bleomycin A5 were identified to contain significantly high amounts of the active forms of caspase‑3 and showed considerable cleavage of poly(ADP‑ribose) polymerase. The mRNA and protein expression levels of the pro‑apoptotic molecule Bcl‑2‑associated X protein were significantly higher in treated NPDFs than in untreated NPDFs. In contrast, the mRNA and protein expression of the anti‑apoptotic molecule B‑cell lymphoma 2 (Bcl‑2) was significantly lower in treated NPDFs. These results indicated that bleomycin A5 could induce apoptosis in primary NPDFs through activation of the Bcl‑2 family and caspase cascades in a time-, and concentration-dependent manner.

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Section: Resultsmentioning

confidence: 99%

Induction of apoptosis in nasal polyp-derived fibroblasts by bleomycin A5 inï¿½vitro

Tian

et al. 2018

Mol Med Report

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“…2 million new cases annually (Sabzichi et al, 2014). First line treatment options are include surgery, then radiation, hormonal therapy, and chemotherapy (Sharifi et al, 2014). Moreover non-selective cytotoxicity of chemotheraputic agents causes adverse effects even irrevocable damages to normal tissues and healthy organisms.…”

Section: Introductionmentioning

confidence: 99%

Silibilin-Induces Apoptosis in Breast Cancer Cells by Modulating p53, p21, Bak and Bcl-xl Pathways

Pirouzpanah¹,

Sabzichi²,

Pirouzpanah³

et al. 2015

Asian Pacific Journal of Cancer Prevention

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Nowadays herbal-derived medicines are attracting attention as new sources of drugs with few side effects. Silibinin is a flavonoid compound with chemotheraputic effects on different cancers such as examples in the prostate, lung, colon and breast. In the present study, the cytotoxic effects of silibinin on MCF7 breast cancer cells were investigated. Apoptosis was determined by flow cytometry and the impact of silibinin on the expression of pivotal genes including Bak, P53, P21, BRCA1, BCL-X1 and ATM was analyzed. Treatment for 24h had a significant dose-dependent inhibitory effect on cell growth (p<0.05) with dose-and time-dependent induction of apoptosis (p<0.05). In addition, there were significant increases in BRCA1, ATM, Bak and Bcl-XL gene expression at the mRNA level with different concentrations of silibinin for 24 or 48 h (p<0.05). Taken together, the results suggest that silibinin inhibits the proliferation and induces apoptosis of MCF-7 cells by down-regulating Bak, P53, P21, BRCA1, BCL-Xl and thus may be considered as an effective adjuvant drug to produce a better chemopreventive response for the cancer therapy.

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“…29 Different strategies have been developed for analysis and study of this cancer. [30][31][32][33] MCF-7 cell line is an excellent in vitro model for studying the mechanisms of chemoresistance as it is susceptible to apoptosis and applied for various investigations on apoptosis or survival of cancer cells. [34][35][36] Although the extensive clinical application of doxorubicin for cancer patients has been studied, its anti-proliferative and death-inducing signalling cascades are yet unclear.…”

Section: Introductionmentioning

confidence: 99%

Doxorubicin Changes Bax /Bcl-xL Ratio, Caspase-8 and 9 in Breast Cancer Cells

Sharifi¹,

Barar²,

Hejazi³

et al. 2015

Adv Pharm Bull

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107

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Roles of the Bcl-2/Bax Ratio, Caspase-8 and 9 in Resistance of Breast Cancer Cells to Paclitaxel

Cited by 89 publications

References 54 publications

Induction of apoptosis in nasal polyp-derived fibroblasts by bleomycin A5 inï¿½vitro

Induction of apoptosis in nasal polyp-derived fibroblasts by bleomycin A5 inï¿½vitro

Silibilin-Induces Apoptosis in Breast Cancer Cells by Modulating p53, p21, Bak and Bcl-xl Pathways

Doxorubicin Changes Bax /Bcl-xL Ratio, Caspase-8 and 9 in Breast Cancer Cells

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