Human GM3 Synthase Attenuates Taxol-Triggered Apoptosis Associated with Downregulation of Caspase-3 in Ovarian Cancer Cells

Huang, Su; Bijangi-Vishehsaraei, Khadijeh; Saadatzadeh, M. Reza; Safa, Ahmad R.

doi:10.4236/jct.2012.35065

Cited by 7 publications

(3 citation statements)

References 28 publications

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“…There are no data in literature on paclitaxel influence upon GM3 expression, but there is the evidence about GM3 attenuation of paclitaxel-triggered apoptosis in ovarian cancer cells. 43 Our finding of decreased apoptosis after combined drug treatment in MDA-MB-231 cell line is in accordance with this reference. 43 …”

Section: Discussionsupporting

confidence: 92%

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Glycophenotype of breast and prostate cancer stem cells treated with thieno[2,3-<em>b</em>]pyridine anticancer compound

Mastelić¹,

Čulić²,

Mužinić³

et al. 2017

DDDT

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Tumor progression may be driven by a small subpopulation of cancer stem cells (CSCs characterized by CD44+/CD24− phenotype). We investigated the influence of a newly developed thienopyridine anticancer compound (3-amino-5-oxo-N-naphthyl-5,6,7, 8-tetrahydrothieno[2,3-b]quinoline-2-carboxamide, 1) on the growth, survival and glycophenotype (CD15s and GM3 containing neuraminic acid substituted with acetyl residue, NeuAc) of breast and prostate cancer stem/progenitor-like cell population. MDA-MB-231 and Du-145 cells were incubated with compound 1 alone or in combination with paclitaxel. The cellular metabolic activity was determined by the 3-(4,5-dimethylthiazolyl-2)-2,5-diphenyltetrazolium bromide (MTT) assay. The type of cell death induced by 48-h treatment was assessed using a combination of Annexin-V-FITC and propidium iodide staining. Flow cytometric analysis was performed to detect the percentage of CD44+/CD24− cells, and GM3 and CD15s positive CSCs, as well as the expression of GM3 and CD15s per one CSC, in both cell lines. Compound 1 produces a dose- and time-dependent cytotoxicity, mediated mainly by apoptosis in breast cancer cells, and slightly (2.3%) but statistically significant lowering breast CSC subpopulation. GM3 expression per one breast CSC was increased, and the percentage of prostate GM3+ CSC subpopulation was decreased in cells treated with compound 1 compared with non-treated cells. The percentage of CD15s+ CSCs was lower in both cell lines after treatment with compound 1. Considering that triple-negative breast cancers are characterized by an increased percentage of breast CSCs and knowing their association with an increased risk of metastasis and mortality, compound 1 is a potentially effective drug for triple-negative breast cancer treatment.

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Section: Discussionsupporting

confidence: 92%

“… 43 Our finding of decreased apoptosis after combined drug treatment in MDA-MB-231 cell line is in accordance with this reference. 43 …”

Section: Discussionsupporting

confidence: 92%

Glycophenotype of breast and prostate cancer stem cells treated with thieno[2,3-<em>b</em>]pyridine anticancer compound

Mastelić¹,

Čulić²,

Mužinić³

et al. 2017

DDDT

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“…Of note, it is worth mentioning that a number of recent papers demonstrated evidence that supports that wild type SKOV3 cells executes taxol-introduced cell death in a caspase-3-dependent manner [51][52][53]. It is well documented that the activation of caspase 3, a main executor protease in apoptosis, is again under heavy influence of various upstream signals coming from both extrinsic (death ligand) and intrinsic (mitochondrial) pathways; some are positive while others are negative regulators depending on the physiological context.…”

Section: Figurementioning

confidence: 99%

Charactor of JNK and P53 in Taxol-Induced Apoptotic Signaling in SKOV3 Human Ovarian Cancer Cell Proliferation

Mostafa¹

2017

JCRCT

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C-Jun N-terminal kinase (JNK) represents a group of mitogen-activated protein kinases (MAPKs) involved in many cellular responses including apoptosis. We have previously reported that taxol, a microtubule-interfering therapeutic agent widely used against various cancers, induces caspase-independent but apoptotic inducing factor (AIF)-dependent apoptosis in human ovarian cancer cell line SKOV3 cells. In the present study, we add to this report a detailed analysis of the taxol-induced apoptotic mechanisms in SKOV3 cells, particularly focusing on JNK and p53. In line with the previous report, we found that taxol induced caspase-independent apoptosis with concurrent activation of JNK, phosphorylation of Bcl-2, Bax translocation to the mitochondria, and AIF release from the mitochondria. Restoration of p53 functionality into SKOV3 cells, which are p53-null cells, by transfection of wild-type p53, however, induced caspase-dependent apoptosis in response to taxol treatment as evidenced by increasing PARP cleavage and the emergence of processed, active caspase-3 and -7. More to the point, treatment with a JNK inhibitor SP600125 blocked taxol-induced apoptotic cell death in both parental SKOV3 cells (p53-deficient) and p53-transfectant cells. Collectively, the aforementioned findings lend support to the view that taxol-induced apoptotic cell death in SKOV3 cells is executed by different mechanisms depending on the presence of p53 but commonly mediated by ASK1-JNK and/or -p38 axes.

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Sialic acids and sialoglycans in endocrinal disorders

Ghosh¹

2020

Sialic Acids and Sialoglycoconjugates in the Biology of Life, Health and Disease

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Human GM3 Synthase Attenuates Taxol-Triggered Apoptosis Associated with Downregulation of Caspase-3 in Ovarian Cancer Cells

Cited by 7 publications

References 28 publications

Glycophenotype of breast and prostate cancer stem cells treated with thieno[2,3-<em>b</em>]pyridine anticancer compound

Glycophenotype of breast and prostate cancer stem cells treated with thieno[2,3-<em>b</em>]pyridine anticancer compound

Charactor of JNK and P53 in Taxol-Induced Apoptotic Signaling in SKOV3 Human Ovarian Cancer Cell Proliferation

Sialic acids and sialoglycans in endocrinal disorders

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