Apoptosis, angiogenesis, inflammation, and oxidative stress: basic interactions in patients with early and metastatic breast cancer

Hamed, Enas A.; Zakhary, Madeha M.; Maximous, Doaa

doi:10.1007/s00432-012-1176-4

Cited by 55 publications

(34 citation statements)

References 40 publications

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“…13 In addition, oxidative stresses are strongly related to apoptosis. [14][15][16] These data may suggest that the tissue deficits are caused in terms of the toxicity of oxLDL along with the involvement of an apoptotic mechanism.…”

Section: Discussionmentioning

confidence: 93%

Imaging Mass Spectrometry Reveals a Decrease of Cardiolipin in the Kidney of NASH Model Mice

2016

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Section: Discussionmentioning

confidence: 93%

Imaging Mass Spectrometry Reveals a Decrease of Cardiolipin in the Kidney of NASH Model Mice

2016

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“…Loss of RGS4 in cancer cells results in aberrant Gβγ-induced Rac activation that is rescued by proteasomal inhibitor or Gβγ scavenger peptide (53,54). Although the causes of RGS4 degradation in advanced breast cancer remain unknown, an interesting observation is that increased angiogenesis and NO production occur at about the same time (55). Nevertheless, additional functions of RGS4 beyond simply accelerating GTPase activity are starting to emerge (56).…”

Section: Figurementioning

confidence: 99%

NO triggers RGS4 degradation to coordinate angiogenesis and cardiomyocyte growth

Jaba¹,

Zhuang²,

Li³

et al. 2013

J. Clin. Invest.

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Myocardial hypertrophy is an adaptation to increased hemodynamic demands. An increase in heart tissue must be matched by a corresponding expansion of the coronary vasculature to maintain and adequate supply of oxygen and nutrients for the heart. The physiological mechanisms that underlie the coordination of angiogenesis and cardiomyocyte growth are unknown. We report that induction of myocardial angiogenesis promotes cardiomyocyte growth and cardiac hypertrophy through a novel NO-dependent mechanism. We used transgenic, conditional overexpression of placental growth factor (PlGF) in murine cardiac tissues to stimulate myocardial angiogenesis and increase endothelial-derived NO release. NO production, in turn, induced myocardial hypertrophy by promoting proteasomal degradation of regulator of G protein signaling type 4 (RGS4), thus relieving the repression of the Gβγ/PI3Kγ/AKT/mTORC1 pathway that stimulates cardiomyocyte growth. This hypertrophic response was prevented by concomitant transgenic expression of RGS4 in cardiomyocytes. NOS inhibitor L-NAME also significantly attenuated RGS4 degradation, and reduced activation of AKT/mTORC1 signaling and induction of myocardial hypertrophy in PlGF transgenic mice, while conditional cardiac-specific PlGF expression in eNOS knockout mice did not induce myocardial hypertrophy. These findings describe a novel NO/RGS4/Gβγ/PI3Kγ/AKT mechanism that couples cardiac vessel growth with myocyte growth and heart size. IntroductionRecent studies have increased appreciation for the relationship between cardiomyocyte growth and angiogenesis and its contribution to molecular regulation of the myocardial hypertrophic response. Myocardial hypertrophy, secondary to increased hemodynamic demands, requires commensurate growth of the coronary vasculature to provide adequate oxygen and nutrients to the increasing cardiac mass; lack of coordination between the myocyte-driven hypertrophic response and the production of angiogenic growth factors hallmarks the transition to heart failure (1). Although vascular endothelium controls a plethora of biological events contributing to cardiovascular homeostasis, including regulation of vascular tone, thrombosis, and myocardial stiffness, little is known about the effect of endothelial signaling on cardiomyocyte growth, regulation of myocardial hypertrophy, and heart size. Our previous observation that a NOS inhibitor, N G -nitro-l-arginine methyl ester (L-NAME), partially prevented angiogenesis-driven myocardial hypertrophy (2) suggests that endothelium-dependent NO production might be responsible for the hypertrophic effect on cardiomyocytes and the increase in heart size.Because there are no known mechanisms that link NO to stimulation of cardiomyocyte hypertrophy, we designed the present study to fill this gap. In cardiomyocytes, G protein-mediated hypertrophic signaling is negatively modulated by regulators of G protein signaling (RGS proteins). Among more than 20 RGS proteins, RGS subtype 4, a GTPase-activating protein for heterotrimeric Gq and ...

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“…Early detection of breast cancer with an accurate and reliable diagnosis procedure causes physicians distinguish benign breast tumors from malignant tumors (2). Breast cancer involved different signaling cascade deregulation (3), and early prognostic markers can could be used for routine diagnosis and patient survival. These biomarkers are able to generate main information related to clinical manner of breast gland tumors (4).…”

Section: Contextmentioning

confidence: 99%

The Role of Interleukin-8 and Its Mechanism in Patients with Breast Cancer: Its Relation with Oxidative Stress and Estrogen Receptor

Sheikhpour

2017

Int J Cancer Manag

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Context: Breast cancer is one of the leading causes of death among women all over the world. Prognostic markers can be used for patient survival. Likewise, these biomarkers are able to generate main information related to clinical manner of breast gland tumors. Interleukin-8 (IL-8) is a chemotactic cytokines caused initiation of an inflammatory response. Evidence Acquisition: We performed a computerized search in Medline/PubMed databases with key words: IL-8, breast cancer, and oxidative stress. Results: IL-8 secretion motivates the expression of adhesion molecule, including fibronectin in human inflammatory breast cancer cells. IL-8 activates PI3K/Akt pathway, which in turn activates NF-κB resulted up-regulation of integrin β3 expression and increases the invasion of breast cancer cells. Therefore, it seems that IL-8/PI3K/Akt/NF-κB/integrin β3 axis may be used for therapeutic intervention of breast cancer with metastasis status. NF-κB plays an important role in IL-8 gene transcription via several signals, such as LPS, TNF-alpha, and oxidative stress. Oxidative stress caused angiogenic factor production, such as vascular endothelial growth factor and IL-8 via cancer cells. Moreover, there is inverse relation between ER level and IL-8, but the mechanism of IL-8 action in estrogen receptor-negative breast cancer is largely unknown. Estrogen receptor and growth factor in breast cancer cells is influenced by mitogen activated protein kinase (MAPK) cascade, as a part of IL-8 signaling pathway. Conclusions: According to these studies, interleukin-8 may be as a main biomarker for breast cancer. It seems that signaling pathway of IL-8 may be used for therapeutic intervention of breast cancer. Also oxidative stress and breast cancer cells with lacking estrogen receptor generate more interleukin-8.

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Apoptosis, angiogenesis, inflammation, and oxidative stress: basic interactions in patients with early and metastatic breast cancer

Cited by 55 publications

References 40 publications

Imaging Mass Spectrometry Reveals a Decrease of Cardiolipin in the Kidney of NASH Model Mice

Imaging Mass Spectrometry Reveals a Decrease of Cardiolipin in the Kidney of NASH Model Mice

NO triggers RGS4 degradation to coordinate angiogenesis and cardiomyocyte growth

The Role of Interleukin-8 and Its Mechanism in Patients with Breast Cancer: Its Relation with Oxidative Stress and Estrogen Receptor

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