bims-almceb Biomed News
on Acute Leukemia Metabolism and Cell Biology
Issue of 2022‒07‒24
nine papers selected by
Camila Kehl Dias
Federal University of Rio Grande do Sul


  1. Front Oncol. 2022 ;12 896426
      Acute myeloid leukemia (AML) is a polyclonal and heterogeneous hematological malignancy. Relapse and refractory after induction chemotherapy are still challenges for curing AML. Leukemia stem cells (LSCs), accepted to originate from hematopoietic stem/precursor cells, are the main root of leukemogenesis and drug resistance. LSCs are dynamic derivations and possess various elusive resistance mechanisms. In this review, we summarized different primary resistance and remolding mechanisms of LSCs after chemotherapy, as well as the indispensable role of the bone marrow microenvironment on LSCs resistance. Through a detailed and comprehensive review of the spectacle of LSCs resistance, it can provide better strategies for future researches on eradicating LSCs and clinical treatment of AML.
    Keywords:  LSCs remolding; acute myeloid leukemia; clonal heterogeneity; drug resistance; leukemia stem cells; resistant mechanisms
    DOI:  https://doi.org/10.3389/fonc.2022.896426
  2. Front Oncol. 2022 ;12 924567
      Acute myeloid leukaemia (AML) is a highly proliferative cancer characterised by infiltration of immature haematopoietic cells in the bone marrow (BM). AML predominantly affects older people and outcomes, particularly in this difficult to treat population remain poor, in part due to inadequate response to therapy, and treatment toxicity. Normal haematopoiesis is supported by numerous support cells within the BM microenvironment or niche, including adipocytes, stromal cells and endothelial cells. In steady state haematopoiesis, haematopoietic stem cells (HSCs) primarily acquire ATP through glycolysis. However, during stress-responses HSCs rapidly transition to oxidative phosphorylation, enabled by mitochondrial plasticity. Historically it was thought that cancer cells preferentially used glycolysis for ATP production, however recently it has become evident that many cancers, including AML primarily use the TCA cycle and oxidative phosphorylation for rapid proliferation. AML cells hijack the stress-response pathways of their non-malignant counterparts, utilising mitochondrial changes to drive expansion. In addition, amino acids are also utilised by leukaemic stem cells to aid their metabolic output. Together, these processes allow AML cells to maximise their ATP production, using multiple metabolites and fuelling rapid cell turnover which is a hallmark of the disease. This review of AML derived changes in the BM niche, which enable enhanced metabolism, will consider the important pathways and discuss future challenges with a view to understanding how AML cells are able to hijack metabolic pathways and how we may elucidate new targets for potential therapies.
    Keywords:  acute myeloid leukaemia; adipocytes; bone marrow niche; free fattty acids; metabolism
    DOI:  https://doi.org/10.3389/fonc.2022.924567
  3. Semin Cancer Biol. 2022 Jul 19. pii: S1044-579X(22)00176-6. [Epub ahead of print]
      Several metabolic pathways for the supply of adenosine triphosphate (ATP) have been proposed; however, the major source of reducing power for ADP in cancer remains unclear. Although glycolysis is the source of ATP in tumors according to the Warburg effect, ATP levels do not differ between cancer cells grown in the presence and absence of glucose. Several theories have been proposed to explain the supply of ATP in cancer, including metabolic reprograming in the tumor microenvironment. However, these theories are based on the production of ATP by the TCA-OxPhos pathway, which is inconsistent with the Warburg effect. We found that blocking fatty acid oxidation (FAO) in the presence of glucose significantly decreased ATP production in various cancer cells. This suggests that cancer cells depend on fatty acids to produce ATP through FAO instead of glycolysis. We observed that cancer cell growth mainly relies on metabolic nutrients and oxygen systemically supplied through the bloodstream instead of metabolic reprogramming. In a spontaneous mouse tumor model (KrasG12D; Pdx1-cre), tumor growth was 2-fold higher in mice fed a high-fat diet (low-carbo diet) that caused obesity, whereas a calorie-balanced, low-fat diet (high-carbo diet) inhibited tumor growth by 3-fold compared with that in mice fed a control/normal diet. This 5-fold difference in tumor growth between mice fed low-fat and high-fat diets suggests that fat-induced obesity promotes cancer growth, and tumor growth depends on fatty acids as the primary source of energy.
    Keywords:  ATP production; cancer energy metabolism; fatty acid oxidation; obesity
    DOI:  https://doi.org/10.1016/j.semcancer.2022.07.005
  4. J Hematol Oncol. 2022 Jul 18. 15(1): 97
      Drug resistance represents a major obstacle in cancer management, and the mechanisms underlying stress adaptation of cancer cells in response to therapy-induced hostile environment are largely unknown. As the central organelle for cellular energy supply, mitochondria can rapidly undergo dynamic changes and integrate cellular signaling pathways to provide bioenergetic and biosynthetic flexibility for cancer cells, which contributes to multiple aspects of tumor characteristics, including drug resistance. Therefore, targeting mitochondria for cancer therapy and overcoming drug resistance has attracted increasing attention for various types of cancer. Multiple mitochondrial adaptation processes, including mitochondrial dynamics, mitochondrial metabolism, and mitochondrial apoptotic regulatory machinery, have been demonstrated to be potential targets. However, recent increasing insights into mitochondria have revealed the complexity of mitochondrial structure and functions, the elusive functions of mitochondria in tumor biology, and the targeting inaccessibility of mitochondria, which have posed challenges for the clinical application of mitochondrial-based cancer therapeutic strategies. Therefore, discovery of both novel mitochondria-targeting agents and innovative mitochondria-targeting approaches is urgently required. Here, we review the most recent literature to summarize the molecular mechanisms underlying mitochondrial stress adaptation and their intricate connection with cancer drug resistance. In addition, an overview of the emerging strategies to target mitochondria for effectively overcoming chemoresistance is highlighted, with an emphasis on drug repositioning and mitochondrial drug delivery approaches, which may accelerate the application of mitochondria-targeting compounds for cancer therapy.
    Keywords:  Cancer drug resistance; Drug repurposing; Mitochondrial adaptation; Mitochondrial dynamics; Mitochondrial transplantation; Mitochondrial-targeted drug delivery
    DOI:  https://doi.org/10.1186/s13045-022-01313-4
  5. J Hematol Oncol. 2022 Jul 21. 15(1): 98
      Mitochondria are essential for tumor growth and progression. However, the heavy demand for mitochondrial activity in cancer leads to increased production of mitochondrial reactive oxygen species (mtROS), accumulation of mutations in mitochondrial DNA, and development of mitochondrial dysfunction. If left unchecked, excessive mtROS can damage and unfold proteins in the mitochondria to an extent that becomes lethal to the tumor. Cellular systems have evolved to combat mtROS and alleviate mitochondrial stress through a quality control mechanism called the mitochondrial unfolded protein response (UPRmt). The UPRmt system is composed of chaperones and proteases, which promote protein folding or eliminate mitochondrial proteins damaged by mtROS, respectively. UPRmt is conserved and activated in cancer in response to mitochondrial stress to maintain mitochondrial integrity and support tumor growth. In this review, we discuss how mitochondria become dysfunctional in cancer and highlight the tumor-promoting functions of key components of the UPRmt.
    Keywords:  Cancer; Mitochondrial chaperonins; Mitochondrial proteases; Mitochondrial proteostasis; Mitochondrial unfolded protein response
    DOI:  https://doi.org/10.1186/s13045-022-01317-0
  6. Cell Mol Life Sci. 2022 Jul 17. 79(8): 428
      The citrate carrier (CIC) is an integral protein of the inner mitochondrial membrane which catalyzes the efflux of mitochondrial citrate (or other tricarboxylates) in exchange with a cytosolic anion represented by a tricarboxylate or a dicarboxylate or phosphoenolpyruvate. In this way, the CIC provides the cytosol with citrate which is involved in many metabolic reactions. Several studies have been carried out over the years on the structure, function and regulation of this metabolite carrier protein both in mammals and in many other organisms. A lot of data on the characteristics of this protein have therefore accumulated over time thereby leading to a complex framework of metabolic and physiological implications connected to the CIC function. In this review, we critically analyze these data starting from the multiple roles played by the mitochondrial CIC in many cellular processes and then examining the regulation of its activity in different nutritional and hormonal states. Finally, the metabolic significance of the citrate flux, mediated by the CIC, across distinct subcellular compartments is also discussed.
    Keywords:  Citrate; Intermediary metabolism; Metabolic network; Metabolite carrier; Mitochondria; Subcellular compartments
    DOI:  https://doi.org/10.1007/s00018-022-04466-0
  7. Eur J Med Chem. 2022 Jul 16. pii: S0223-5234(22)00515-3. [Epub ahead of print]240 114613
      Metabolic reprogramming is now considered as one of hallmark of tumor cells and provides them with a selective survival/growth advantage to resist harsh micro-environmental stress. Fatty acid (FA) metabolism of tumor cells supports the biosynthetic needs and provides fuel sources for energy supply. Since FA metabolic reprogramming is a critical link in tumor metabolism, its various roles in tumors have attracted increasing interest. Herein, we review the mechanisms through which cancer cells rewire their FA metabolism with a focus on the pathway of FA metabolism and its targeting drug development. The failure and successful cases of targeting tumor FA metabolism are expected to bypass the metabolic vulnerability and improve the efficacy of targeted therapy.
    Keywords:  Fatty acid; Metabolic reprograming; Targeted drug; Tumor metabolism
    DOI:  https://doi.org/10.1016/j.ejmech.2022.114613
  8. Future Oncol. 2022 Jul 19.
      Prevention of relapse is a major therapeutic challenge and an unmet need for patients with acute myeloid leukemia (AML). Venetoclax is a highly selective, potent, oral BCL-2 inhibitor that induces apoptosis in AML cells. When combined with azacitidine, it leads to prolonged overall survival and rapid, durable remissions in treatment-naive AML patients ineligible for intensive chemotherapy. VIALE-M is a randomized, double-blind, two-arm study to evaluate the safety and efficacy of venetoclax in combination with oral azacitidine (CC-486) as maintenance therapy in patients in complete remission with incomplete blood count recovery after intensive induction and consolidation therapies. The primary end point is relapse-free survival. Secondary outcomes include overall survival, minimal residual disease conversion and improvement in quality-of-life. Trial registration number: NCT04102020 (ClinicalTrials.gov).
    Keywords:  BCL-2 inhibitor; CC-486 (oral azacitidine); acute myeloid leukemia; first remission; maintenance therapy; minimal residual disease conversion; phase III; relapse-free survival; venetoclax
    DOI:  https://doi.org/10.2217/fon-2022-0450