bims-almceb Biomed News
on Acute Leukemia Metabolism and Cell Biology
Issue of 2023–01–08
nine papers selected by
Camila Kehl Dias, Federal University of Rio Grande do Sul



  1. Adv Exp Med Biol. 2022 ;1393 103-124
      Microenvironment of cancer stem cells (CSCs) consists of a variety of cells and inter-cellular matrix and communications of the components. The microenvironment of CSCs maintains the stemness feature of the CSCs. Several cell types which communicate each other via signaling molecules surrounding CSCs are main factors of the CSC microenvironment. A key question is "What kind of information the cells exchange in the CSC microenvironment?" to reveal the microenvironment and CSC features. Components and molecular markers of CSC microenvironment, signaling cross-talks in CSC microenvironment, and targeting CSC microenvironment are focused in this review.
    Keywords:  Cancer stem cell; Microenvironment; Signaling pathway
    DOI:  https://doi.org/10.1007/978-3-031-12974-2_5
  2. Adv Exp Med Biol. 2022 ;1393 125-139
      Many tumors are resistant to conventional cancer therapies because a tumor is composed of heterogeneous cell population. Especially, subpopulation of cancer stem cells, which have self-renewal and differentiation properties and responsible for the tumor initiation, is generally considered resistant to chemo-, radio-, and immune therapy. Understanding the mechanism of drug resistance in cancer stem cells should lead to establish more effective therapeutic strategies. Actually, different molecular mechanisms are conceivable for cancer stem cells acquiring drug resistance. These mechanisms include not only cytoplasmic signaling pathways but also the intercellular communications in the tumor microenvironment. Recently, a great deal of successful reports challenged to elucidate the mechanisms of drug resistance and to develop novel treatments targeting cancer stem cells.
    Keywords:  Cancer stem cells; Drug resistance; Signal pathways; Treatments
    DOI:  https://doi.org/10.1007/978-3-031-12974-2_6
  3. Front Pharmacol. 2022 ;13 1106129
      
    Keywords:  anti-cancer immunity; biomarker; combination therapy; immunotherapy; therapeutic toxicity
    DOI:  https://doi.org/10.3389/fphar.2022.1106129
  4. Cancer Sci. 2023 Jan 05.
      To meet cellular bioenergetic and biosynthetic demands, cancer cells remodel their metabolism to increase glycolytic flux, a phenomenon known as the Warburg effect and believed to contribute to cancer malignancy. Among glycolytic enzymes, phosphofructokinase-1 (PFK1) has been shown to act as a rate-limiting enzyme and to facilitate the Warburg effect in cancer cells. In this study, however, we found that decreased PFK1 activity did not affect cell survival or proliferation in cancer cells. This raised a question regarding the importance of PFK1 in malignancy. To gain insights into the role of PFK1 in cancer metabolism and the possibility of adopting it as a novel anti-cancer therapeutic target, we screened for genes that caused lethality when they were knocked down in the presence of tryptolinamide (TLAM), a PFK1 inhibitor. The screen revealed a synthetic chemical-genetic interaction between genes encoding subunits of ATP synthase (complex V) and TLAM. Indeed, after TLAM treatment, the sensitivity of HeLa cells to oligomycin A (OMA), an ATP synthase inhibitor, was 13,000 times higher than that of untreated cells. Furthermore, this sensitivity potentiation by TLAM treatment was recapitulated by genetic mutations of PFK1. By contrast, TLAM did not potentiate the sensitivity of normal fibroblast cell lines to OMA, possibly due to their reduced energy demands compared to cancer cells. We also showed that the PFK1-mediated glycolytic pathway can act as an energy reservoir. Selective potentiation of the efficacy of ATP synthase inhibitors by PFK1 inhibition may serve as a foundation for novel anti-cancer therapeutic strategies.
    Keywords:  ATP synthase; PFK1; Warburg effect; glycolysis; shRNA screening
    DOI:  https://doi.org/10.1111/cas.15713
  5. Immunol Rev. 2023 Jan 02.
      Hematopoietic stem cells (HSCs) and multipotent progenitor cells (MPPs) arise in successive waves during ontogeny, and their properties change significantly throughout life. Ontological changes in HSCs/MPPs underlie corresponding changes in mechanisms of pediatric leukemia initiation. As HSCs and MPPs progress from fetal to neonatal, juvenile and adult stages of life, they undergo transcriptional and epigenetic reprogramming that modifies immune output to meet age-specific pathogenic challenges. Some immune cells arise exclusively from fetal HSCs/MPPs. We propose that this layered immunity instructs cell fates that underlie a parallel layered leukemogenicity. Indeed, some pediatric leukemias, such as juvenile myelomonocytic leukemia, myeloid leukemia of Down syndrome, and infant pre-B-cell acute lymphoblastic leukemia, are age-restricted. They only present during infancy or early childhood. These leukemias likely arise from fetal progenitors that lose competence for transformation as they age. Other childhood leukemias, such as non-infant pre-B-cell acute lymphoblastic leukemia and acute myeloid leukemia, have mutation profiles that are common in childhood but rare in morphologically similar adult leukemias. These differences could reflect temporal changes in mechanisms of mutagenesis or changes in how progenitors respond to a given mutation at different ages. Interactions between leukemogenic mutations and normal developmental switches offer potential targets for therapy.
    Keywords:  age-biased mutation profiles; age-restricted leukemias; layered immunity; pediatric leukemia
    DOI:  https://doi.org/10.1111/imr.13180
  6. Cell Metab. 2023 Jan 03. pii: S1550-4131(22)00546-0. [Epub ahead of print]35(1): 3-5
      Metabolic communication in the tumor microenvironment underscores tumor-immune interactions and affects anti-tumor immunity, yet cell-extrinsic signals driving tumor metabolic remodeling are incompletely understood. In this issue, Tsai et al. show that during initial tumorigenesis, T cell-derived IFNγ triggers STAT3 activation and c-Myc-dependent alterations of tumor cell metabolism, which potentiates immune evasion.
    DOI:  https://doi.org/10.1016/j.cmet.2022.12.009
  7. Front Pharmacol. 2022 ;13 1009952
      Warburg effect is characterized by excessive consumption of glucose by the tumor cells under both aerobic and hypoxic conditions. This metabolic reprogramming allows the tumor cells to adapt to the unique microenvironment and proliferate rapidly, and also promotes tumor metastasis and therapy resistance. Metabolic reprogramming of tumor cells is driven by the aberrant expression and activity of metabolic enzymes, which results in the accumulation of oncometabolites, and the hyperactivation of intracellular growth signals. Recent studies suggest that tumor-associated metabolic remodeling also depends on intercellular communication within the tumor microenvironment (TME). Small extracellular vesicles (sEVs), also known as exosomes, are smaller than 200 nm in diameter and are formed by the fusion of multivesicular bodies with the plasma membrane. The sEVs are instrumental in transporting cargoes such as proteins, nucleic acids or metabolites between the tumor, stromal and immune cells of the TME, and are thus involved in reprogramming the glucose metabolism of recipient cells. In this review, we have summarized the biogenesis and functions of sEVs and metabolic cargos, and the mechanisms through they drive the Warburg effect. Furthermore, the potential applications of targeting sEV-mediated metabolic pathways in tumor liquid biopsy, imaging diagnosis and drug development have also been discussed.
    Keywords:  drug development; exosomes; glycolysis; liquid biopsy; small extracellular vesicles; tumor metabolism; warburg effect
    DOI:  https://doi.org/10.3389/fphar.2022.1009952
  8. Front Oncol. 2022 ;12 1091782
      Immune evasion through up-regulating checkpoint inhibitory receptors on T cells plays an essential role in tumor initiation and progression. Therefore, immunotherapy, including immune checkpoint inhibitor targeting programmed cell death protein 1 (PD-1) and chimeric antigen receptor T cell (CAR-T) therapy, has become a promising strategy for hematological malignancies. T cell immunoreceptor with immunoglobulin and ITIM domain (TIGIT) is a novel checkpoint inhibitory receptor expressed on immune cells, including cytotoxic T cells, regulatory T cells, and NK cells. TIGIT participates in immune regulation via binding to its ligand CD155. Blockage of TIGIT has provided evidence of considerable efficacy in solid tumors in preclinical research and clinical trials, especially when combined with PD-1 inhibition. However, the mechanism and function of TIGIT in hematological malignancies have not been comprehensively studied. In this review, we focus on the role of TIGIT in hematological malignancies and discuss therapeutic strategies targeting TIGIT, which may provide a promising immunotherapy target for hematological malignancies.
    Keywords:  TIGIT; hematological malignancy; immunotherapy; leukemia; lymphoma; multiple myeloma
    DOI:  https://doi.org/10.3389/fonc.2022.1091782
  9. Front Oncol. 2022 ;12 1007565
       Problems: γδ T cells are essential for anti-leukemia function in immunotherapy, however, γδ T cells have different functional subsets, including regulatory cell subsets expressing the Foxp3. Whether they are correlated with immune-checkpoint mediated T cell immune dysfunction remains unknown in patients with acute myeloid leukemia (AML).
    Methods: In this study, we used RNA-seq data from 167 patients in TCGA dataset to analyze the correlation between PD-1 and FOXP3 genes and these two genes' association with the prognosis of AML patients. The expression proportion of Foxp3+/PD-1+ cells in γδ T cells and two subgroups Vδ1 and Vδ2 T cells were performed by flow cytometry. The expression level of FOXP3 and PD-1 genes in γδ T cells were sorted from peripheral blood by MACS magnetic cell sorting technique were analyzed by quantitative real-time PCR.
    Results: We found that PD-1 gene was positively correlated with FOXP3 gene and highly co-expressed PD-1 and FOXP3 genes were associated with poor overall survival (OS) from TCGA database. Then, we detected a skewed distribution of γδ T cells with increased Vδ1 and decreased Vδ2 T cell subsets in AML. Moreover, significantly higher percentages of PD-1+ γδ, Foxp3+ γδ, and PD-1+Foxp3+ γδ T cells were detected in de novo AML patients compared with healthy individuals. More importantly, AML patients containing higher PD-1+Foxp3+ γδ T cells had lower OS, which might be a potential therapeutic target for leukemia immunotherapy.
    Conclusion: A significant increase in the PD-1+Foxp3+ γδ T cell subset in AML was associated with poor clinical outcome, which provides predictive value for the study of AML patients.
    Keywords:  Foxp3; PD-1; acute myeloid leukemia; outcome; overall survival; γδ T cells
    DOI:  https://doi.org/10.3389/fonc.2022.1007565