Targeting Metabolism: A Potential Strategy for Hematological Cancer Therapy

Overview

Journal World J Clin Cases

Publisher Baishideng Publishing Group

Specialty General Medicine

Date 2022 Jun 1

PMID 35647127

Authors

Xue Tang

Fen Chen

Li-Chun Xie

Si-Xi Liu

Hui-Rong Mai

Affiliations

Soon will be listed here.

Abstract

Most hematological cancer-related relapses and deaths are caused by metastasis; thus, the importance of this process as a target of therapy should be considered. Hematological cancer is a type of cancer in which metabolism plays an essential role in progression. Therefore, we are required to block fundamental metastatic processes and develop specific preclinical and clinical strategies against those biomarkers involved in the metabolic regulation of hematological cancer cells, which do not rely on primary tumor responses. To understand progress in this field, we provide a summary of recent developments in the understanding of metabolism in hematological cancer and a general understanding of biomarkers currently used and under investigation for clinical and preclinical applications involving drug development. The signaling pathways involved in cancer cell metabolism are highlighted and shed light on how we could identify novel biomarkers involved in cancer development and treatment. This review provides new insights into biomolecular carriers that could be targeted as anticancer biomarkers.

References

Watson C, Long J, Orange C, Tannahill C, Mallon E, McGlynn L . High expression of sphingosine 1-phosphate receptors, S1P1 and S1P3, sphingosine kinase 1, and extracellular signal-regulated kinase-1/2 is associated with development of tamoxifen resistance in estrogen receptor-positive breast cancer patients. Am J Pathol. 2010; 177(5):2205-15. PMC: 2966780. DOI: 10.2353/ajpath.2010.100220. View

Koch S, Claesson-Welsh L . Signal transduction by vascular endothelial growth factor receptors. Cold Spring Harb Perspect Med. 2012; 2(7):a006502. PMC: 3385940. DOI: 10.1101/cshperspect.a006502. View

Oeckinghaus A, Ghosh S . The NF-kappaB family of transcription factors and its regulation. Cold Spring Harb Perspect Biol. 2010; 1(4):a000034. PMC: 2773619. DOI: 10.1101/cshperspect.a000034. View

Park M, Hong J . Roles of NF-κB in Cancer and Inflammatory Diseases and Their Therapeutic Approaches. Cells. 2016; 5(2). PMC: 4931664. DOI: 10.3390/cells5020015. View

Matolay O, Mehes G . Sustain, Adapt, and Overcome-Hypoxia Associated Changes in the Progression of Lymphatic Neoplasia. Front Oncol. 2019; 9:1277. PMC: 6881299. DOI: 10.3389/fonc.2019.01277. View

Mendoza M, Er E, Blenis J . The Ras-ERK and PI3K-mTOR pathways: cross-talk and compensation. Trends Biochem Sci. 2011; 36(6):320-8. PMC: 3112285. DOI: 10.1016/j.tibs.2011.03.006. View

Chapuis N, Tamburini J, Green A, Vignon C, Bardet V, Neyret A . Dual inhibition of PI3K and mTORC1/2 signaling by NVP-BEZ235 as a new therapeutic strategy for acute myeloid leukemia. Clin Cancer Res. 2010; 16(22):5424-35. DOI: 10.1158/1078-0432.CCR-10-1102. View

Bertacchini J, Guida M, Accordi B, Mediani L, Martelli A, Barozzi P . Feedbacks and adaptive capabilities of the PI3K/Akt/mTOR axis in acute myeloid leukemia revealed by pathway selective inhibition and phosphoproteome analysis. Leukemia. 2014; 28(11):2197-205. DOI: 10.1038/leu.2014.123. View

Palazon A, Goldrath A, Nizet V, Johnson R . HIF transcription factors, inflammation, and immunity. Immunity. 2014; 41(4):518-28. PMC: 4346319. DOI: 10.1016/j.immuni.2014.09.008. View

10.

Iommarini L, Porcelli A, Gasparre G, Kurelac I . Non-Canonical Mechanisms Regulating Hypoxia-Inducible Factor 1 Alpha in Cancer. Front Oncol. 2017; 7:286. PMC: 5711814. DOI: 10.3389/fonc.2017.00286. View

11.

Fayard E, Moncayo G, Hemmings B, Hollander G . Phosphatidylinositol 3-kinase signaling in thymocytes: the need for stringent control. Sci Signal. 2010; 3(135):re5. DOI: 10.1126/scisignal.3135re5. View

12.

Lainey E, Wolfromm A, Sukkurwala A, Micol J, Fenaux P, Galluzzi L . EGFR inhibitors exacerbate differentiation and cell cycle arrest induced by retinoic acid and vitamin D3 in acute myeloid leukemia cells. Cell Cycle. 2013; 12(18):2978-91. PMC: 3875673. DOI: 10.4161/cc.26016. View

13.

Laplante M, Sabatini D . mTOR signaling in growth control and disease. Cell. 2012; 149(2):274-93. PMC: 3331679. DOI: 10.1016/j.cell.2012.03.017. View

14.

Mahmud H, Kornblau S, Ter Elst A, Scherpen F, Qiu Y, Coombes K . Epidermal growth factor receptor is expressed and active in a subset of acute myeloid leukemia. J Hematol Oncol. 2016; 9(1):64. PMC: 4971659. DOI: 10.1186/s13045-016-0294-x. View

15.

Sun S, Cesarman E . NF-κB as a target for oncogenic viruses. Curr Top Microbiol Immunol. 2010; 349:197-244. PMC: 3855473. DOI: 10.1007/82_2010_108. View

16.

Regad T . Targeting RTK Signaling Pathways in Cancer. Cancers (Basel). 2015; 7(3):1758-84. PMC: 4586793. DOI: 10.3390/cancers7030860. View

17.

Masson N, Ratcliffe P . Hypoxia signaling pathways in cancer metabolism: the importance of co-selecting interconnected physiological pathways. Cancer Metab. 2014; 2(1):3. PMC: 3938304. DOI: 10.1186/2049-3002-2-3. View

18.

Fang Y, Yang Y, Hua C, Xu S, Zhou M, Guo H . Rictor has a pivotal role in maintaining quiescence as well as stemness of leukemia stem cells in MLL-driven leukemia. Leukemia. 2016; 31(2):414-422. DOI: 10.1038/leu.2016.223. View

19.

Santarpia L, Lippman S, El-Naggar A . Targeting the MAPK-RAS-RAF signaling pathway in cancer therapy. Expert Opin Ther Targets. 2012; 16(1):103-19. PMC: 3457779. DOI: 10.1517/14728222.2011.645805. View

20.

Ding W, Knox T, Tschumper R, Wu W, Schwager S, Boysen J . Platelet-derived growth factor (PDGF)-PDGF receptor interaction activates bone marrow-derived mesenchymal stromal cells derived from chronic lymphocytic leukemia: implications for an angiogenic switch. Blood. 2010; 116(16):2984-93. PMC: 2974606. DOI: 10.1182/blood-2010-02-269894. View