Cancer cells change their glucose metabolism to overcome increased ROS: One step from cancer cell to cancer stem cell?

Movahed, Zahra Ghanbari; Rastegari-Pouyani, Mohsen; Mohammadi, Mohammad Hossein; Mansouri, Kamran

doi:10.1016/j.biopha.2019.108690

Cited by 143 publications

(92 citation statements)

References 185 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…CD44 (CD44v) expression in CSCs suppresses PKM2 (mice model), thereby decreasing pyruvate dehydrogenase activity and promoting PPP; these are all consistent with the stabilization of the cysteine/glutamate antiporter and elevated GSH levels (58,(60)(61)(62). All these lead to higher survival rates of CSC even in hostile environments (15,57,58). In isolated CRC, miR-124, miR-137, and miR-340 have been reported as being able to switch the Warburg effect's glycolytic mechanism into one involving oxidative phosphorylation in CRCs, which impairs cancer growth as a result (63).…”

Section: Metabolism Characteristics Of Csc That Enhance Invasivenessmentioning

confidence: 67%

“…Interestingly, the Warburg effect and the enhancement of the PPP in CSCs seem to be responsible for the enhanced production of antioxidant molecules and the overall reduction of reactive oxygen species (ROS) demonstrated in vivo and in vitro models (15,55,59). CD44 (CD44v) expression in CSCs suppresses PKM2 (mice model), thereby decreasing pyruvate dehydrogenase activity and promoting PPP; these are all consistent with the stabilization of the cysteine/glutamate antiporter and elevated GSH levels (58,(60)(61)(62). All these lead to higher survival rates of CSC even in hostile environments (15,57,58).…”

Section: Metabolism Characteristics Of Csc That Enhance Invasivenessmentioning

confidence: 92%

“…Therefore, fulfillment of much of the energy requirements comes from glycolysis, which is the fastest energy-producing pathway (52-54) due to the Warburg effect that is characterized by high pyruvate and low lactate production (55)(56)(57). Furthermore, the high volume of glycolysis intermediates is then used in the pentose phosphate pathway (PPP) to produce ribose, which is necessary for nucleotide synthesis and in anabolic reactions for lipid synthesis (56,58).…”

Section: Metabolism Characteristics Of Csc That Enhance Invasivenessmentioning

confidence: 99%

See 2 more Smart Citations

Colorectal Cancer Stem Cells in the Progression to Liver Metastasis

et al. 2020

View full text Add to dashboard Cite

Colorectal carcinoma (CRC) is a leading cause of cancer mortality. Tumorigenesis is a dynamic process wherein cancer stem cells (CSCs) and their microenvironment promote initiation, progression, and metastasis. Metastatic colonization is an inefficient process that is very complex and is poorly understood; however, in most cases, metastatic disease is not curable, and resistance mechanisms tend to develop against conventional treatments. An understanding of the underlying mechanisms and factors that contribute to the development of metastasis in CRC can aid in the search for specific therapeutic targets for improving standard treatments. In this review, we summarize current knowledge regarding tumor biology and the use of stroma cells as prognostic factors and inflammatory inducers associated with the use of tumor microenvironments as a promoter of cancer metastasis. Moreover, we look into the importance of CSC, pericytes, and circulating tumor cells as mechanisms that lead to liver metastasis, and we also focus on the cellular and molecular pathways that modulate and regulate epithelial-mesenchymal transition. Finally, we discuss a novel therapeutic target that can potentially eliminate CSCs as a CRC treatment.

show abstract

Section: Metabolism Characteristics Of Csc That Enhance Invasivenessmentioning

confidence: 67%

Section: Metabolism Characteristics Of Csc That Enhance Invasivenessmentioning

confidence: 92%

Section: Metabolism Characteristics Of Csc That Enhance Invasivenessmentioning

confidence: 99%

See 1 more Smart Citation

Colorectal Cancer Stem Cells in the Progression to Liver Metastasis

et al. 2020

View full text Add to dashboard Cite

show abstract

“…Recently it has been shown that cells maintain the ability to switch between metabolic phenotypes very rapidly and use both OXPHOS and glycolysis mechanisms to overcome hostile environments in the body and even develop resistance to drugs (171). For example the initial accumulation of ROS drives cancer cells to switch from OXPHOS to glycolysis, but chronic ROS exposure rewires metabolism toward the pentose phosphate pathway with cells undergoing a stem-like phenotype that's more resistant to therapies (172). Lactate and pyruvate, the byproducts of glycolysis, regulate hypoxia-inducible factor 1α (HIF-1α) and Wnt signaling independently of oxygen availability, which in turn alters iron metabolism (34).…”

Section: Metabolic Plasticitymentioning

confidence: 99%

Altered Iron Metabolism and Impact in Cancer Biology, Metastasis, and Immunology

et al. 2020

View full text Add to dashboard Cite

Iron is an essential nutrient that plays a complex role in cancer biology. Iron metabolism must be tightly controlled within cells. Whilst fundamental to many cellular processes and required for cell survival, excess labile iron is toxic to cells. Increased iron metabolism is associated with malignant transformation, cancer progression, drug resistance and immune evasion. Depleting intracellular iron stores, either with the use of iron chelating agents or mimicking endogenous regulation mechanisms, such as microRNAs, present attractive therapeutic opportunities, some of which are currently under clinical investigation. Alternatively, iron overload can result in a form of regulated cell death, ferroptosis, which can be activated in cancer cells presenting an alternative anti-cancer strategy. This review focuses on alterations in iron metabolism that enable cancer cells to meet metabolic demands required during different stages of tumorigenesis in relation to metastasis and immune response. The strength of current evidence is considered, gaps in knowledge are highlighted and controversies relating to the role of iron and therapeutic targeting potential are discussed. The key question we address within this review is whether iron modulation represents a useful approach for treating metastatic disease and whether it could be employed in combination with existing targeted drugs and immune-based therapies to enhance their efficacy.

show abstract

“…For instance, PDIA1 mitochondrial localization contributes to the induction of mitochondrial outer membrane permeabilization (MOMP), the release of the mitochondrial cytochrome c into the cytoplasm and the initiation of apoptosis ( 15 ). Furthermore, PDIA1 mitochondrial localization suggested that this protein is involved in the regulation of redox mediated mitochondrial functions including energy metabolism ( 16 ). Nuclear localization of PDIA1 implicated this protein in the regulation of the activity of redox-sensitive transcription factors to co-ordinate efficient ROS detoxification ( 17 ).…”

Section: Introductionmentioning

confidence: 99%

Protein disulfide isomerase A1 regulates breast cancer cell immunorecognition in a manner dependent on redox state

et al. 2020

View full text Add to dashboard Cite

Oxidoreductase protein disulphide isomerases (PDI) are involved in the regulation of a variety of biological processes including the modulation of endoplasmic reticulum (ER) stress, unfolded protein response (UPR), ER-mitochondria communication and the balance between pro-survival and pro-death pathways. In the current study the role of the PDIA1 family member in breast carcinogenesis was investigated by measuring ROS generation, mitochondrial membrane disruption, ATP production and HLA-G protein levels on the surface of the cellular membrane in the presence or absence of PDIA1. The results showed that this enzyme exerted pro-apoptotic effects in estrogen receptor (ERα)-positive breast cancer MCF-7 and pro-survival in triple negative breast cancer (TNBC) MDA-MB-231 cells. ATP generation was upregulated in PDIA1 -silenced MCF-7 cells and downregulated in PDIA1 -silenced MDA-MB-231 cells in a manner dependent on the cellular redox status. Furthermore, MCF-7 and MDA-MB-231 cells in the presence of PDIA1 expressed higher surface levels of the non-classical human leukocyte antigen (HLA-G) under oxidative stress conditions. Evaluation of the METABRIC datasets showed that low PDIA1 and high HLA-G mRNA expression levels correlated with longer survival in both ERα-positive and ERα-negative stage 2 breast cancer patients. In addition, analysis of the PDIA1 vs. the HLA-G mRNA ratio in the subgroup of the living stage 2 breast cancer patients exhibiting low PDIA1 and high HLA-G mRNA levels revealed that the longer the survival time of the ratio was high PDIA1 and low HLA-G mRNA and occurred predominantly in ERα-positive breast cancer patients whereas in the same subgroup of the ERα-negative breast cancer mainly this ratio was low PDIA1 and high HLA-G mRNA. Taken together these results provide evidence supporting the view that PDIA1 is linked to several hallmarks of breast cancer pathways including the process of antigen processing and presentation and tumor immunorecognition.

show abstract

Cancer cells change their glucose metabolism to overcome increased ROS: One step from cancer cell to cancer stem cell?

Cited by 143 publications

References 185 publications

Colorectal Cancer Stem Cells in the Progression to Liver Metastasis

Colorectal Cancer Stem Cells in the Progression to Liver Metastasis

Altered Iron Metabolism and Impact in Cancer Biology, Metastasis, and Immunology

Protein disulfide isomerase A1 regulates breast cancer cell immunorecognition in a manner dependent on redox state

Contact Info

Product

Resources

About