Exosomal circCARM1 from spheroids reprograms cell metabolism by regulating PFKFB2 in breast cancer

Oncogene ◽  
2022 ◽  
Author(s):  
Yonglei Liu ◽  
Li Ma ◽  
Fanli Hua ◽  
Zhihui Min ◽  
Yanxia Zhan ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Metabolism

scholarly journals DDR1 Affects Metabolic Reprogramming in Breast Cancer Cells by Cross-Talking to the Insulin/IGF System

Biomolecules ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 926
Author(s):  
Veronica Vella ◽  
Marika Giuliano ◽  
Maria Luisa Nicolosi ◽  
Maria Giovanna Majorana ◽  
Małgorzata Anna Marć ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Breast Cancer Cells ◽  
Cell Metabolism ◽  
Growth Factor Receptor ◽  
Metabolic Reprogramming ◽  
Atp Production ◽  
Igf System ◽  
Putative Target ◽  
Collagen Receptor ◽  
Discoidin Domain Receptor 1

The insulin receptor isoform A (IR-A), a dual receptor for insulin and IGF2, plays a role in breast cancer (BC) progression and metabolic reprogramming. Notably, discoidin domain receptor 1 (DDR1), a collagen receptor often dysregulated in cancer, is involved in a functional crosstalk and feed forward loop with both the IR-A and the insulin like growth factor receptor 1 (IGF1R). Here, we aimed at investigating whether DDR1 might affect BC cell metabolism by modulating the IGF1R and/or the IR. To this aim, we generated MCF7 BC cells engineered to stably overexpress either IGF2 (MCF7/IGF2) or the IR-A (MCF7/IR-A). In both cell models, we observed that DDR1 silencing induced a significant decrease of total ATP production, particularly affecting the rate of mitochondrial ATP production. We also observed the downregulation of key molecules implicated in both glycolysis and oxidative phosphorylation. These metabolic changes were not modulated by DDR1 binding to collagen and occurred in part in the absence of IR/IGF1R phosphorylation. DDR1 silencing was ineffective in MCF7 knocked out for DDR1. Taken together, these results indicate that DDR1, acting in part independently of IR / IGF1R stimulation, might work as a novel regulator of BC metabolism and should be considered as putative target for therapy in BC.

scholarly journals Suppression of PDHX by microRNA-27b deregulates cell metabolism and promotes growth in breast cancer

2018 ◽  
Vol 17 (1) ◽  
Author(s):  
Steven C. Eastlack ◽  
Shengli Dong ◽  
Cristina Ivan ◽  
Suresh K. Alahari
Keyword(s):  
Breast Cancer ◽  
Cell Metabolism

Radiosensitizing effects of citrate-coated cobalt and nickel ferrite nanoparticles on breast cancer cells

Nanomedicine ◽  
2020 ◽  
Vol 15 (29) ◽  
pp. 2823-2836
Author(s):  
Daniele A Fagundes ◽  
Liliam V Leonel ◽  
Luis E Fernandez-Outon ◽  
José D Ardisson ◽  
Raquel G dos Santos
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Nickel Ferrite ◽  
Breast Cancer Cells ◽  
Cell Metabolism ◽  
Ferrite Nanoparticles ◽  
Normal Fibroblast ◽  
Normal Cells ◽  
Nickel Ferrite Nanoparticles ◽  
Cobalt And Nickel

Aim: Evaluation of the biocompatibility and radiosensitizer potential of citrate-coated cobalt (cit-CF) and nickel (cit-NF) ferrite nanoparticles (NPs). Materials & methods: Normal fibroblast and breast cancer cells were treated with different concentrations of citrate-coated ferrite NPs (cit-NPs) and irradiated with a cobalt-60 source at doses of 1 and 3 Gy. After 24 h, cell metabolism, morphology alterations and nanoparticle uptake were evaluated. Results: Cit-CF and cit-NF NPs showed no toxicity to normal cells up to 250 and 100 μg.ml-1, respectively. Combination of cit-NP and ionizing radiation resulted in up to fivefold increase in the radiation therapeutic efficacy against breast cancer cells. Conclusion: Cit-CF and cit-NF NPs are suitable candidates for application as breast cancer cell radiosensitizers.

scholarly journals The landscape of tiered regulation of breast cancer cell metabolism

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Rotem Katzir ◽  
Ibrahim H. Polat ◽  
Michal Harel ◽  
Shir Katz ◽  
Carles Foguet ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Metabolic Regulation ◽  
Cell Metabolism ◽  
Cancer Cell Line ◽  
Hierarchical Organization ◽  
Metabolic Reprogramming ◽  
A Genome ◽  
Cancer Cell Metabolism

AbstractAltered metabolism is a hallmark of cancer, but little is still known about its regulation. In this study, we measure transcriptomic, proteomic, phospho-proteomic and fluxomics data in a breast cancer cell-line (MCF7) across three different growth conditions. Integrating these multiomics data within a genome scale human metabolic model in combination with machine learning, we systematically chart the different layers of metabolic regulation in breast cancer cells, predicting which enzymes and pathways are regulated at which level. We distinguish between two types of reactions, directly and indirectly regulated. Directly-regulated reactions include those whose flux is regulated by transcriptomic alterations (~890) or via proteomic or phospho-proteomics alterations (~140) in the enzymes catalyzing them. We term the reactions that currently lack evidence for direct regulation as (putative) indirectly regulated (~930). Many metabolic pathways are predicted to be regulated at different levels, and those may change at different media conditions. Remarkably, we find that the flux of predicted indirectly regulated reactions is strongly coupled to the flux of the predicted directly regulated ones, uncovering a tiered hierarchical organization of breast cancer cell metabolism. Furthermore, the predicted indirectly regulated reactions are predominantly reversible. Taken together, this architecture may facilitate rapid and efficient metabolic reprogramming in response to the varying environmental conditions incurred by the tumor cells. The approach presented lays a conceptual and computational basis for mapping metabolic regulation in additional cancers.

scholarly journals MicroRNA and Oxidative Stress Interplay in the Context of Breast Cancer Pathogenesis

2019 ◽  
Vol 20 (20) ◽  
pp. 5143 ◽  
Author(s):  
Giulia Cosentino ◽  
Ilaria Plantamura ◽  
Alessandra Cataldo ◽  
Marilena V. Iorio
Keyword(s):  
Breast Cancer ◽  
Oxidative Stress ◽  
Cancer Progression ◽  
Genome Instability ◽  
Pathological Condition ◽  
Cell Metabolism ◽  
Comprehensive Overview ◽  
Ros Signaling ◽  
Cancer Pathogenesis ◽  
Regulatory Functions

Oxidative stress is a pathological condition determined by a disturbance in reactive oxygen species (ROS) homeostasis. Depending on the entity of the perturbation, normal cells can either restore equilibrium or activate pathways of cell death. On the contrary, cancer cells exploit this phenomenon to sustain a proliferative and aggressive phenotype. In fact, ROS overproduction or their reduced disposal influence all hallmarks of cancer, from genome instability to cell metabolism, angiogenesis, invasion and metastasis. A persistent state of oxidative stress can even initiate tumorigenesis. MicroRNAs (miRNAs) are small non coding RNAs with regulatory functions, which expression has been extensively proven to be dysregulated in cancer. Intuitively, miRNA transcription and biogenesis are affected by the oxidative status of the cell and, in some instances, they participate in defining it. Indeed, it is widely reported the role of miRNAs in regulating numerous factors involved in the ROS signaling pathways. Given that miRNA function and modulation relies on cell type or tumor, in order to delineate a clearer and more exhaustive picture, in this review we present a comprehensive overview of the literature concerning how miRNAs and ROS signaling interplay affects breast cancer progression.

scholarly journals Somatic Mutation of PIK3CA (H1047R) Is a Common Driver Mutation Hotspot in Canine Mammary Tumors as Well as Human Breast Cancers

Cancers ◽  
2019 ◽  
Vol 11 (12) ◽  
pp. 2006 ◽  
Author(s):  
Kang-Hoon Lee ◽  
Hyeon-Ji Hwang ◽  
Hyun Ji Noh ◽  
Tae-Jin Shin ◽  
Je-Yoel Cho
Keyword(s):  
Breast Cancer ◽  
Human Cancer ◽  
Association Studies ◽  
Cell Metabolism ◽  
Driver Mutations ◽  
Genome Wide Association Studies ◽  
Breast Cancers ◽  
Human Breast ◽  
Normal Tissues ◽  
Whole Exome

Breast cancer is one of the most frequently diagnosed cancers in both women and female dogs. Genome-wide association studies in human breast cancer (HBC) have identified hundreds of genetic variations and somatic driver mutations. However, only a handful of variants have been studied for rare HBC and their associations remain inconclusive. Spontaneous canine mammary tumor (CMT) is a great model for HBC, with clinical similarity. We thus performed whole-exome sequencing in 20 pairs of CMT and normal tissues in dogs. We newly found that PIK3CA was the most frequently mutated gene in CMT (45%). Furthermore, canine PIK3CA A3140G (H1047R), at what is known as the mutational hotspot of HBC, is also a hotspot in CMT. Targeted sequencing confirmed that 29% of CMTs had the same PIK3CA A3140G mutation. Integration of the transcriptome suggests that the PIK3CA (H1047R) induced cell metabolism and cell cycle via an increase of PCK2 and a decrease of CDKN1B but had no effect on cell apoptosis. We identified additional significantly mutated genes, including SCRN1 and CLHC1, which have not been reported in HBC. Our study recapitulated some known HBC-associated genes and human cancer signatures in CMT, and identified novel genes that may be relevant to HBC. This study may allow us to better understand both HBC and CMT and lend new insights into the development of biomarkers.

scholarly journals Autofluorescence flow sorting of breast cancer cell metabolism

2016 ◽  
Vol 10 (8) ◽  
pp. 1026-1033 ◽  
Author(s):  
Amy T. Shah ◽  
Taylor M. Cannon ◽  
James N. Higginbotham ◽  
Robert J. Coffey ◽  
Melissa C. Skala
Keyword(s):  
Breast Cancer ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cell Metabolism ◽  
Flow Sorting ◽  
Cancer Cell Metabolism
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