Involvement of 15-lipoxygenase-1 in the regulation of breast cancer cell death induced by sodium butyrate

Salimi, Vahid; Shabani, Mohammad; Nourbakhsh, Mitra; Tavakoli-Yaraki, Masoumeh

doi:10.1007/s10616-016-9972-3

Cited by 15 publications

(15 citation statements)

References 34 publications

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“…To address this, we set up a connected set of experiments to characterize the possible anticancer effect of sodium butyrate on breast cancer cell growth as well as normal breast cells. The results of the current study also our previous study [ 20 ] have revealed that sodium butyrate deceased the rate of viable breast cancer cells in a dose and time dependent manner. In our previous study the involvement of 15-lipoxygenase in the regulation of breast cancer cell growth induced by sodium butyrate was explored [ 20 ], however in the present study the exact mechanism underlying sodium butyrate-induced cell death in human breast cancer is perused.…”

Section: Discussionsupporting

confidence: 90%

“…The results of the current study also our previous study [ 20 ] have revealed that sodium butyrate deceased the rate of viable breast cancer cells in a dose and time dependent manner. In our previous study the involvement of 15-lipoxygenase in the regulation of breast cancer cell growth induced by sodium butyrate was explored [ 20 ], however in the present study the exact mechanism underlying sodium butyrate-induced cell death in human breast cancer is perused. In support of this, the appropriate range of sodium butyrate concentrations (0.1–20 mM) at different time intervals were investigated.…”

Section: Discussionsupporting

confidence: 90%

“…The combination of lower doses of sodium butyrate with a pro-apoptotic agents might help to favor the benefits of sodium butyrate in induction of apoptosis. We have shown that 15-lipoxygenase product has synergistic effect with sodium butyrate in induction of toxicity in breast cancer cells [ 20 ]. Our results were in line with previous studies about the effectiveness of sodium butyrate on breast cancer cell regulation [ 9 , 28 – 30 ], however our study aimed to investigate complete panel of elements which might be involved in the induction of apoptosis insisting on the role of mitochondria and ROS which were not considered in the previous studies.…”

Section: Discussionmentioning

confidence: 99%

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Sodium butyrate promotes apoptosis in breast cancer cells through reactive oxygen species (ROS) formation and mitochondrial impairment

et al. 2017

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BackgroundSodium butyrate (NaBu) is a short-chain fatty acid which serves as a histon deacetylase inhibitor and has received considerable interest as a possible regulator of cancer cell death. The regulatory effect of NaBu on cancer cell growth or death has yet to be illustrated in many cancers including breast cancer. This study is aimed to elucidate the possible effect of NaBu on regulation of breast cancer growth and apoptosis.MethodsThe cytotoxic effect of NaBu on the growth of breast cancer cells (MCF-7 and MDA-MB-468) and normal breast cells (MCF-10A) was determined using MTT assay. Annexin-V-FITC staining and PI staining were performed to detect apoptosis and cell cycle distribution using Flow cytometry, the level of mitochondrial membrane potential (Δψm), Reactive oxygen species (ROS)formation and caspase activity were determined accordingly.ResultsBased on our data, NaBu induced a dose and time-dependent cell toxicity in breast cancer cells which was related to the cell cycle arrest and induction of apoptosis. The impact of NaBu on MCF-10A cell toxicity, cell cycle distribution and apoptosis was inconsiderable. NaBu-elicited apoptosis was accompanied by the elevated level of ROS, increased caspase activity and reduced mitochondrial membrane potential (Δψm) in MCF-7 and MDA-MB-468 cells and with no effect on the above mentioned factors in MCF-10A cells.ConclusionsOur study provided insight in to the role of NaBu on the regulation of breast cancer cell growth and lighten up the pro-apoptotic activity of NaBu.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

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Sodium butyrate promotes apoptosis in breast cancer cells through reactive oxygen species (ROS) formation and mitochondrial impairment

et al. 2017

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“…Although NaB was found be beneficial to several diseases (He et al 2016, Li et al 2016, Salimi et al 2016, Subramanian et al 2016, little is known about its protection against DN. To the best of our knowledge, there has been only one study that reported NaB protection against DN (Khan & Jena 2014).…”

Section: Discussionmentioning

confidence: 99%

Sodium butyrate activates NRF2 to ameliorate diabetic nephropathy possibly via inhibition of HDAC

Dong

Jia

Liu

et al. 2017

Journal of Endocrinology

119

100

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Oxidative stress contributes to the pathogenesis of diabetic nephropathy (DN). Nuclear factor erythroid 2-related factor 2 (NRF2) plays a key role in cellular defense against oxidative stress. NRF2 activators have shown promising preventive effects on DN. Sodium butyrate (NaB) is a known activator of NRF2. However, it is unknown whether NRF2 is required for NaB protection against DN. Therefore, streptozotocin-induced diabetic C57BL/6 Nrf2 knockout and their wild-type mice were treated in the presence or absence of NaB for 20 weeks. Diabetic mice, but not NaB-treated diabetic mice, developed significant renal oxidative damage, inflammation, apoptosis, fibrosis, pathological changes and albuminuria. NaB inhibited histone deacetylase (HDAC) activity and elevated the expression of Nrf2 and its downstream targets heme oxygenase 1 and NAD(P)H dehydrogenase quinone 1. Notably, deletion of the Nrf2 gene completely abolished NaB activation of NRF2 signaling and protection against diabetes-induced renal injury. Interestingly, the expression of Kelch-like ECH-associated protein 1, the negative regulator of NRF2, was not altered by NaB under both diabetic and non-diabetic conditions. Moreover, NRF2 nuclear translocation was not promoted by NaB. Therefore, the present study indicates, for the first time, that NRF2 plays a key role in NaB protection against DN. Other findings suggest that NaB may activate Nrf2 at the transcriptional level, possibly by the inhibition of HDAC activity.

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“…The protection conferred by HDAC inhibition may be associated with the upregulation of histone acetylation at the promoter region of nfe2l2. NaB, a natural short-chain fatty acid, is an HDAC inhibitor that affects proliferation, differentiation, and apoptosis of cell (83). Dong et al demonstrated that NaB may activate Nfe2l2 at the transcriptional level to ameliorate DN possibly by inhibiting HDAC activity (60).…”

Section: Epigenetic Modifications Of Nrf2 By Pharmacological Agentsmentioning

confidence: 99%

NRF2-Related Epigenetic Modifications in Cardiac and Vascular Complications of Diabetes Mellitus

et al. 2021

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Diabetes mellitus (DM) is a highly prevalent chronic disease that is accompanied with serious complications, especially cardiac and vascular complications. Thus, there is an urgent need to identify new strategies to treat diabetic cardiac and vascular complications. Nuclear factor erythroid 2-related factor 2 (NRF2) has been verified as a crucial target for the prevention and treatment of diabetic complications. The function of NRF2 in the treatment of diabetic complications has been widely reported, but the role of NRF2-related epigenetic modifications remains unclear. The purpose of this review is to summarize the recent advances in targeting NRF2-related epigenetic modifications in the treatment of cardiac and vascular complications associated with DM. We also discuss agonists that could potentially regulate NRF2-associated epigenetic mechanisms. This review provides a better understanding of strategies to target NRF2 to protect against DM-related cardiac and vascular complications.

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Involvement of 15-lipoxygenase-1 in the regulation of breast cancer cell death induced by sodium butyrate

Cited by 15 publications

References 34 publications

Sodium butyrate promotes apoptosis in breast cancer cells through reactive oxygen species (ROS) formation and mitochondrial impairment

Sodium butyrate promotes apoptosis in breast cancer cells through reactive oxygen species (ROS) formation and mitochondrial impairment

Sodium butyrate activates NRF2 to ameliorate diabetic nephropathy possibly via inhibition of HDAC

NRF2-Related Epigenetic Modifications in Cardiac and Vascular Complications of Diabetes Mellitus

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