Tamoxifen - DEBIO 1143 kombinasyonunun östrojen reseptörü pozitif meme kanseri hücre hatlarındaki etkisi.

Tuğrul, Berrin; Işseven, Merve

doi:10.31362/patd.623005

Cited by 2 publications

(1 citation statement)

References 55 publications

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“…Tamoxifen citrate could inhibit the protein kinase C activity and is implicated as an anticancer drug as it has a significant role as a selective estrogen response modifier, and also an anti-angiogenic factor [56]. This drug can mitigate breast cancer progression [57][58][59]. However, the tamoxifen-resistance is one of the significant aspects in breast cancer cells and the resistant mechanisms are being maintained by the recurrent activation of Nrf2-mediated antioxidant response elements in breast cancer cells through ERK signaling [60].…”

Section: Plos Onementioning

confidence: 99%

Screening fructosamine-3-kinase (FN3K) inhibitors, a deglycating enzyme of oncogenic Nrf2: Human FN3K homology modelling, docking and molecular dynamics simulations

Beeraka,

Zhang,

Mandal

et al. 2023

PLoS ONE

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Fructosamine-3-kinase (FN3K) is involved in the deglycation of Nrf2, a significant regulator of oxidative stress in cancer cells. However, the intricate functional aspects of FN3K and Nrf2 in breast cancers have not been explored vividly. The objectives of this study are to design the human FN3K protein using homology modeling followed by the screening of several anticancer molecules and examining their efficacy to modulate FN3K activity, Nrf2-mediated antioxidant signalling. Methods pertinent to homology modeling, virtual screening, molecular docking, molecular dynamics simulations, assessment of ADME properties, cytotoxicity assays for anticancer molecules of natural/synthetic origin in breast cancer cells (BT-474, T-47D), and Western blotting were used in this study. The screened anticancer molecules including kinase inhibitors of natural and synthetic origin interacted with the 3-dimensional structure of the catalytic domain in human FN3K protein designed through homology modeling by significant CDOCKER interaction energies. Subsequently, gefitinib, sorafenib, neratinib, tamoxifen citrate, and cyclosporine A enhanced the expression of FN3K in BT-474 cell lines with simultaneous alteration in Nrf2-driven antioxidant signalling. Oxaliplatin significantly downregulated FN3K expression and modulated Nrf2-driven antioxidant signalling when compared to cisplatin and other anticancer drugs. Hence, the study concluded the potential implications of existing anticancer drugs to modulate FN3K activity in breast cancers.

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Section: Plos Onementioning

confidence: 99%

Screening fructosamine-3-kinase (FN3K) inhibitors, a deglycating enzyme of oncogenic Nrf2: Human FN3K homology modelling, docking and molecular dynamics simulations

Beeraka,

Zhang,

Mandal

et al. 2023

PLoS ONE

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Cytotoxic effect of DEBIO 1143 on Triple Negative Mouse Breast Cancer Cell Lines by Non-Apoptosis Death Mechanisms

Tuğrul,

Alp,

Balcan

2023

Preprint

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Background Triple negative breast cancer (TNBC) is a lethal cancer lacking therapeutic targets. In this project, we aimed to investigate the cytotoxic effect of DEBIO 1143, a SMAC mimetic, on 4T1 and 4T1-HER2 mouse TNBC cell lines and the cell death pathway through which this effect is mediated. Methods and results MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) test was used to determine cell viability, flow cytometry analysis was performed to determine apoptosis, and MDC (monodansylcadaverine) was used to determine autophagic vesicles. In addition, LC3II, Beclin 1, RIP3 and cIAP1 proteins were analyzed by western blot. In both cell lines, it was determined that DEBIO 1143 IC50 doses caused predominantly non-apoptotic cell death in the 48-h drug-treated group. In western blot analysis, LC3II level was significantly increased in 4T1-HER2 cells treated with DEBIO 1143 for 24 and 48 hours compared to control. Beclin 1 expression was significantly elevated in the drug treatment groups of both cell lines. The expression level of RIP3 in 4T1 cells was relatively increased after 24 and 48 h treatment of DEBIO 1143 compared to control. cIAP1 protein bands were detected in both control and 24- h treatment groups of both cell lines, but not in 48- h treatment groups. Conclusions Our findings revealed that DEBIO 1143 showed a time-dependent cytotoxic effect in mouse TNBC cell lines. This effect may be predominantly mediated through non-apoptosis cell death mechanisms such as autophagy and necrosis. Further research is recommended to clarify the issue fully.

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Tamoxifen - DEBIO 1143 kombinasyonunun östrojen reseptörü pozitif meme kanseri hücre hatlarındaki etkisi.

Abstract: The effect of DEBIO 1143 usage alone or in combination with tamoxifen on estrogen receptor positive breast cancer cell lines DEBIO 1143'ün tek başına veya tamoxifenle kombinasyonunun östrojen reseptörü pozitif meme kanseri hücre hatlarındaki etkisi

Cited by 2 publications

References 55 publications

Screening fructosamine-3-kinase (FN3K) inhibitors, a deglycating enzyme of oncogenic Nrf2: Human FN3K homology modelling, docking and molecular dynamics simulations

Screening fructosamine-3-kinase (FN3K) inhibitors, a deglycating enzyme of oncogenic Nrf2: Human FN3K homology modelling, docking and molecular dynamics simulations

Cytotoxic effect of DEBIO 1143 on Triple Negative Mouse Breast Cancer Cell Lines by Non-Apoptosis Death Mechanisms

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