Prognostic value of CEC count in HER2-negative metastatic breast cancer patients treated with bevacizumab and chemotherapy: a prospective validation study (UCBG COMET)

Vasseur, Antoine; Cabel, Luc; Trédan, Olivier; Chevrier, Marion; Dubot, Coraline; Lorgis, Véronique; Jacot, William; Gonçalvès, Anthony; Debled, Marc; Lévy, Christelle; Ferrero, Jean-­Marc; Jouannaud, Christelle; Luporsi, É.; Mouret-Reynier, Marie-Ange; Lemonnier, Jérôme; Savignoni, Alexia; Tanguy, Marie‐Laure; Bidard, François‐Clément; Pierga, Jean‐Yves

doi:10.1007/s10456-019-09697-7

Cited by 11 publications

(9 citation statements)

References 33 publications

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“…The cells were then incubated with primary antibodies at 4°C overnight followed by incubation with secondary antibodies for 1 h at RT [ 40 ]. Then, the samples were stained with DAPI, mounted on slides, and photographed using the Olympus microscope at 200x magnification [ 41 , 42 ]. The average fluorescence intensity was calculated using Image J software.…”

Section: Methodsmentioning

confidence: 99%

[Retracted] Irisin Attenuates Oxidative Stress, Mitochondrial Dysfunction, and Apoptosis in the H9C2 Cellular Model of Septic Cardiomyopathy through Augmenting Fundc1‐Dependent Mitophagy

Jiang

Cai

Jin

et al. 2021

Oxidative Medicine and Cellular Longevity

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In the present study, we used lipopolysaccharide- (LPS-) stimulated H9C2 cardiomyocytes to investigate whether irisin treatment attenuates septic cardiomyopathy via Fundc1-related mitophagy. Fundc1 levels and mitophagy were significantly reduced in LPS-stimulated H9C2 cardiomyocytes but were significantly increased by irisin treatment. Irisin significantly increased ATP production and the activities of mitochondrial complexes I and III in the LPS-stimulated cardiomyocytes. Irisin also improved glucose metabolism and significantly reduced LPS-induced levels of reactive oxygen species by increasing the activities of antioxidant enzymes, glutathione peroxidase (GPX), and superoxide dismutase (SOD), as well as levels of reduced glutathione (GSH). TUNEL assays showed that irisin significantly reduced LPS-stimulated cardiomyocyte apoptosis by suppressing the activation of caspase-3 and caspase-9. However, the beneficial effects of irisin on oxidative stress, mitochondrial metabolism, and viability of LPS-stimulated H9C2 cardiomyocytes were abolished by silencing Fundc1. These results demonstrate that irisin abrogates mitochondrial dysfunction, oxidative stress, and apoptosis through Fundc1-related mitophagy in LPS-stimulated H9C2 cardiomyocytes. This suggests irisin is a potentially useful treatment for septic cardiomyopathy, though further investigations are necessary to confirm our findings.

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Section: Methodsmentioning

confidence: 99%

[Retracted] Irisin Attenuates Oxidative Stress, Mitochondrial Dysfunction, and Apoptosis in the H9C2 Cellular Model of Septic Cardiomyopathy through Augmenting Fundc1‐Dependent Mitophagy

Jiang

Cai

Jin

et al. 2021

Oxidative Medicine and Cellular Longevity

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“…Furthermore, its nitrate effect generates NO free radicals, which directly activate the guanylate cyclase and increase cGMP synthesis in myocardial microcirculation. Elevated cGMP levels, in turn, target cGMP-dependent kinases and cyclic nucleotide-gated ion channel effectors [ 89 – 91 ]. Reduced intracellular free Ca 2+ and desensitization of smooth muscle cell contractile proteins to Ca 2+ result in vasodilation, decreased vascular resistance, and widening of blood vessels [ 92 ].…”

Section: Effects Of Nicorandil On Mitochondrial Integritymentioning

confidence: 99%

[Retracted] Protective Effect of Nicorandil on Cardiac Microvascular Injury: Role of Mitochondrial Integrity

Jiang

et al. 2021

Oxidative Medicine and Cellular Longevity

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A major shortcoming of postischemic therapy for myocardial infarction is the no-reflow phenomenon due to impaired cardiac microvascular function including microcirculatory barrier function, loss of endothelial activity, local inflammatory cell accumulation, and increased oxidative stress. Consequently, inadequate reperfusion of the microcirculation causes secondary ischemia, aggravating the myocardial reperfusion injury. ATP-sensitive potassium ion (KATP) channels regulate the coronary blood flow and protect cardiomyocytes from ischemia-reperfusion injury. Studies in animal models of myocardial ischemia-reperfusion have illustrated that the opening of mitochondrial KATP (mito-KATP) channels alleviates endothelial dysfunction and reduces myocardial necrosis. By contrast, blocking mito-KATP channels aggravates microvascular necrosis and no-reflow phenomenon following ischemia-reperfusion injury. Nicorandil, as an antianginal drug, has been used for ischemic preconditioning (IPC) due to its mito-KATP channel-opening effect, thereby limiting infarct size and subsequent severe ischemic insult. In this review, we analyze the protective actions of nicorandil against microcirculation reperfusion injury with a focus on improving mitochondrial integrity. In addition, we discuss the function of mitochondria in the pathogenesis of myocardial ischemia.

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“…State 4 (leak) respiration was assessed with the complex V inhibitor oligomycin (2 μg/mL). Respiration due to reactive oxygen species formation was assessed with Antimycin A (2.5 μm) [31]. O 2 flux was measured by Datlab2 software (Oroboros Instruments, Innsbruck, Austria), capable of converting nonlinear changes in the negative time derivative of the oxygen concentration signal [32].…”

Section: Mitochondrial Respiration Assaysmentioning

confidence: 99%

Yap-Hippo Signaling Activates Mitochondrial Protection and Sustains Breast Cancer Viability under Hypoxic Stress

Chen

Zhang

Guo

et al. 2021

Journal of Oncology

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Yes-associated protein (Yap) is a transcriptional regulator that upregulates oncogenes and downregulates tumor repressor genes. In this study, we analyzed protein expression, RNA transcription, and signaling pathways to determine the function and mechanism of Yap in breast cancer survival during hypoxic stress. Yap transcription was drastically upregulated by hypoxia in a time-dependent manner. siRNA-mediated Yap knockdown attenuated breast cancer viability and impaired cell proliferation under hypoxic conditions. Yap knockdown induced mitochondrial stress, including mitochondrial membrane potential reduction, mitochondrial oxidative stress, and ATP exhaustion after exposure to hypoxia. It also repressed mitochondrial protective systems, including mitophagy and mitochondrial fusion upon exposure to hypoxia. Finally, our data showed that Yap knockdown suppresses MCF-7 cell migration by inhibiting F-actin transcription and promoting lamellipodium degradation under hypoxic stress. Taken together, Yap maintenance of mitochondrial function and activation of F-actin/lamellipodium signaling is required for breast cancer survival, migration, and proliferation under hypoxic stress.

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Prognostic value of CEC count in HER2-negative metastatic breast cancer patients treated with bevacizumab and chemotherapy: a prospective validation study (UCBG COMET)

Cited by 11 publications

References 33 publications

[Retracted] Irisin Attenuates Oxidative Stress, Mitochondrial Dysfunction, and Apoptosis in the H9C2 Cellular Model of Septic Cardiomyopathy through Augmenting Fundc1‐Dependent Mitophagy

[Retracted] Irisin Attenuates Oxidative Stress, Mitochondrial Dysfunction, and Apoptosis in the H9C2 Cellular Model of Septic Cardiomyopathy through Augmenting Fundc1‐Dependent Mitophagy

[Retracted] Protective Effect of Nicorandil on Cardiac Microvascular Injury: Role of Mitochondrial Integrity

Yap-Hippo Signaling Activates Mitochondrial Protection and Sustains Breast Cancer Viability under Hypoxic Stress

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