BackgroundThe transfer of whole mitochondria that occurs during cell contact has been found to support cancer progression. However, the regulatory role of mitochondria alone is difficult to elucidate due to the complex microenvironment. Currently, mitochondrial transplantation is an available approach for restoring mitochondrial function in mitochondrial diseases but remains unclear in breast cancer. Herein, effects of mitochondrial transplantation via different approaches in breast cancer were investigated.MethodsWhole mitochondria (approximately 10.5 μg/ml) were transported into MCF-7 breast cancer cells via passive uptake or Pep-1-mediated delivery. Fresh mitochondria isolated from homeoplasmic 143B osteosarcoma cybrids containing mitochondrial DNA (mtDNA) derived from health individuals (Mito) or mtDNA with the A8344G mutation (Mito8344) were conjugated with cell-penetrating peptide Pep-1 (P-Mito) or not conjugated prior to cell co-culture. Before isolation, mitochondria were stained with MitoTracker dye as the tracking label. After 3 days of treatment, cell viability, proliferation, oxidative stress, drug sensitivity to Doxorubicin/Paclitaxel and mitochondrial function were assessed.ResultsCompared with P-Mito, a small portion of Mito adhered to the cell membrane, and this was accompanied by a slightly lower fluorescent signal by foreign mitochondria in MCF-7 cells. Both transplantations induced cell apoptosis by increasing the nuclear translocation of apoptosis-inducing factor; inhibited cell growth and decreased oxidative stress in MCF-7 cells; and increased the cellular susceptibility of both the MCF-7 and MDA-MB-231 cell lines to Doxorubicin and Paclitaxel. Mitochondrial transplantation also consistently decreased Drp-1, which resulted in an enhancement of the tubular mitochondrial network, but a distinct machinery through the increase of parkin and mitochondrial fusion proteins was observed in the Mito and P-Mito groups, respectively. Furthermore, although there were no differences in energy metabolism after transplantation of normal mitochondria, metabolism was switched to the energetic and glycolytic phenotypes when the mitochondria were replaced with dysfunctional mitochondria, namely, Mito8344 and P-Mito8344, due to dramatically induced glycolysis and reduced mitochondrial respiration, respectively. Consequently, transplant-induced growth inhibition was abolished, and cell growth in the Mito8344 group was even higher than that in the control group.ConclusionThis study reveals the antitumour potential of mitochondrial transplantation in breast cancer via distinct regulation of mitochondrial function.Electronic supplementary materialThe online version of this article (10.1186/s13046-019-1028-z) contains supplementary material, which is available to authorized users.

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A high-performance graphite-Si composite anode for Li-ion batteries containing Si nanoparticles (NPs) attached onto graphite microparticles was synthesized by adopting a polymer-blend of poly(diallyl dimethyl-ammonium chloride) and poly(sodium 4-styrenesulfonate). The polymer-blend enabled uniform distribution of Si NPs during synthesis and served as a robust artificial solid-electrolyte interphase that substantially enhanced the cycle stability and rate performance of the composite electrode. The electrode exhibited a specific capacity of 450 mA h g(-1), 96% capacity retention at a 10 C-rate, 95% retention after 200 cycles, and the same electrode expansion behavior as a pristine graphite electrode.

MRI tends to overestimate the actual tumor size, while sonography frequently underestimates it. Combined sonography and MRI increases the accuracy of tumor size prediction.

BackgroundAdipokines, including adipocyte fatty acid-binding protein (A-FABP), have been demonstrated to be involved in the pathogenesis of atherosclerosis. In the present study, we investigated the association of circulating A-FABP level with severity of myocardial perfusion abnormalities analyzed by Tl-201 dipyridamole single-photon emission computed tomography.MethodsA total of 170 patients with coronary artery disease (CAD) from cardiovascular clinics were enrolled in the study. Serum A-FABP levels, echocardiography, and stress myocardial perfusion imaging results were analyzed.ResultsCompared with the patients with mild CAD (summed stress score [SSS] ≤ 8), those with moderate to severe CAD (SSS > 8) had significantly higher A-FABP concentrations. However, the difference was attenuated in the subgroup of patients with heart failure. In the correlation analyses, A-FABP level was correlated with age, body mass index, waist circumference, levels of creatinine, fasting glucose, high-sensitivity C-reactive protein, N-terminal pro-brain natriuretic peptide, adiponectin, and several echocardiographic parameters, including left ventricular ejection fraction. Multivariate logistic regression analysis demonstrated that the A-FABP level was not only associated with higher SSS (odds ratio, 1.30; 95% confidence interval [CI], 1.01–1.69; P = 0.048), but also an independent risk factor for heart failure (odds ratio 2.71, 95% CI, 1.23–5.94; P = 0.013).ConclusionsSerum A-FABP levels not only were associated with myocardial perfusion abnormalities and left ventricular function, but also predicted the presence of heart failure in our patients with CAD.

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