Glucocorticoid Receptor Activation Inhibits p53-induced Apoptosis of MCF10Amyc Cells via Induction of Protein Kinase Cϵ

Aziz, Moammir H.; Maki, Carl G.

doi:10.1074/jbc.m112.393256

Cited by 23 publications

(15 citation statements)

References 49 publications

(61 reference statements)

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“…Moreover, these opposing effects seem to be cell‐type specific, although their precise mechanisms remain unclear. For example, GR can induce apoptosis in immune, multiple myeloma and brain cells, but it inhibits apoptosis in other cell types such as hepatocytes and endothelial and epithelial cells . In the present study, we demonstrated that mice with increased heat tolerance exhibited increased mitochondrial GR in skeletal muscle.…”

Section: Discussionsupporting

confidence: 59%

Glucocorticoid receptor activation is associated with increased resistance to heat‐induced hyperthermia and injury

Chen

2017

Acta Physiologica

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Section: Discussionsupporting

confidence: 59%

Glucocorticoid receptor activation is associated with increased resistance to heat‐induced hyperthermia and injury

Chen

2017

Acta Physiologica

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“…This process inhibits production of the tumor suppressor protein PDCD4, while enhancing the expression of antiapoptosis genes and anticancer drug resistance in MCF-7 cells [38]. In addition, activation of glucocorticoid receptor (GR) by stimulating GR agonists, such as hydrocortisone and dexamethasone, can inhibit p53-dependent apoptosis of breast cancer cells through an increase in the levels of PKC messenger RNA (mRNA) and protein [64]. PKC can also protect breast cancer cells from major death factor tumor necrosis factor (TNF )-induced cell death through DNA-dependent protein kinase-mediated Akt activation [65], Akt-dependent murine double minute 2 activation, and p53 downregulation [66].…”

Section: Pkc Isozymes and Cancermentioning

confidence: 99%

Protein Kinase C (PKC) Isozymes and Cancer

Kang

2014

New Journal of Science

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Protein kinase C (PKC) is a family of phospholipid-dependent serine/threonine kinases, which can be further classified into three PKC isozymes subfamilies: conventional or classic, novel or nonclassic, and atypical. PKC isozymes are known to be involved in cell proliferation, survival, invasion, migration, apoptosis, angiogenesis, and drug resistance. Because of their key roles in cell signaling, PKC isozymes also have the potential to be promising therapeutic targets for several diseases, such as cardiovascular diseases, immune and inflammatory diseases, neurological diseases, metabolic disorders, and multiple types of cancer. This review primarily focuses on the activation, mechanism, and function of PKC isozymes during cancer development and progression.

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“…43 This might be an important antiapoptotic mechanism in the retina, as DEX prevented photoreceptor death without improving the MFP-induced Bcl-X L depletion.…”

Section: Early Effects Of Dex and Mfpmentioning

confidence: 99%

Mifepristone, a Blocker of Glucocorticoid Receptors, Promotes Photoreceptor Death

Cubilla¹,

Bermúdez²,

Marquioni-Ramella³

et al. 2013

Invest. Ophthalmol. Vis. Sci.

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PURPOSE. Glucocorticoids are best known by their protective effect on retinal photoreceptor damage. However, they could also be involved in photoreceptor homeostasis under basal, nonstressful conditions. Therefore, we aimed to study glucocorticoid-induced changes of survival-related molecules in male mice retinas under standard illumination conditions (12 hours light, 60 lux/12 h dark).METHODS. Male Balb-c mice were injected with dexamethasone (DEX), a selective glucocorticoid receptor a (GRa) agonist, its antagonist mifepristone (MFP), or both drugs (DþM) at noon. A group of mice was subjected to surgical adrenalectomy (AdrX). Retinas were studied by histology, immunohistochemistry, TUNEL procedure, and Western blotting at different periods after pharmacological or surgical intervention (6 hours, 48 hours, or 7 days). RESULTS.The antiapoptotic molecule Bcl-X L significantly increased 6 hours after DEX injection. By contrast, this molecule could no longer be found after MFP injection. At the same time, high levels of cleaved caspase-3 (CC-3) and Bax appeared in retinal extracts, and TUNEL þ nuclei selectively showed in the outer nuclear layer (ONL). After MFP, retinal extracts also contained phosphorylated histone H2AX (p-H2AX), a marker of DNA breakage and repair. Loss of ONL nuclear rows and decrease of rhodopsin levels were evident 7 days after MFP administration. These changes were minimized when DEX was given together with MFP (DþM). In the absence of MFP, DEX increased Bcl-X L in every retinal layer, with a marked intensification in photoreceptor inner segments. Numerous TUNEL þ nuclei rapidly appeared in the ONL after AdrX. CONCLUSIONS.A single dose of MFP induced selective photoreceptor damage in the absence of other environmental stressors. Because damage was prevented by DEX, and was reproduced by AdrX, our findings suggest that glucocorticoids play a critical role in photoreceptor survival. (Invest Ophthalmol Vis Sci. 2013;54:313-322)

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Glucocorticoid Receptor Activation Inhibits p53-induced Apoptosis of MCF10Amyc Cells via Induction of Protein Kinase Cϵ

Cited by 23 publications

References 49 publications

Glucocorticoid receptor activation is associated with increased resistance to heat‐induced hyperthermia and injury

Glucocorticoid receptor activation is associated with increased resistance to heat‐induced hyperthermia and injury

Protein Kinase C (PKC) Isozymes and Cancer

Mifepristone, a Blocker of Glucocorticoid Receptors, Promotes Photoreceptor Death

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