Targeting Metabolic Cross Talk between Cancer Cells and Cancer-Associated Fibroblasts

  • Jin G. Jung
  • Anne LeEmail author
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 1063)


Although tumorigenesis has classically been regarded as a genetic disease of uncontrolled cell growth, the importance of the tumor microenvironment (TME) is continuously emphasized by the accumulating evidence that cancer growth is not simply dependent on the cancer cells themselves [1, 2] but also dependent on angiogenesis [3–6], inflammation [7, 8], and the supporting roles of cancer-associated fibroblasts (CAFs) [9, 10]. After the discovery that CAFs are able to remodel the tumor matrix within the TME and provide the nutrients and chemicals to promote cancer cell growth [11], many studies have aimed to uncover the cross talk between cancer and CAFs. Moreover, a new paradigm in cancer metabolism shows how cancer cells act like “metabolic parasites” to uptake the high-energy metabolites, such as lactate, ketone bodies, free fatty acid, and glutamine from supporting cells, including CAFs and cancer-associated adipocytes (CAAs) [12, 13]. This chapter provides an overview of the metabolic coupling between CAFs and cancer to further define the therapeutic options to disrupt the CAF-cancer cell interactions.


Cancer-associated fibroblasts Cancer-associated adipocytes Tumor microenvironment Metabolism Metabolites Cancer therapy 





Acetyl-CoA acetyltransferase


Acetyl-CoA carboxylase


Alpha-cyano-4-hydroxycinnamic acid


ATP citrate lyase


Alanine, serine, cysteine-preferring transporter 2


3-Hydroxybutyrate dehydrogenase 1


Cancer-associated adipocytes


Cancer-associated fibroblasts




Extracellular matrix


Epidermal growth factor


Fatty acid synthase






Human growth hormone




3-Hydroxy-3-methylglutaryl-CoA synthase 2


Heat-shock protein 60


Lysophosphatidic acid


Monocarboxylate transporter 1


Monocarboxylate transporter 4


Matrix metalloprotease


Oxidative phosphorylation


Phosphatidic acid


Phosphoinositide 3-kinase


Phosphatidylinositol (3,4,5)-trisphosphate


Phosphatase and tensin homolog deleted on chromosome 10




Tricarboxylic acid


Tumor microenvironment


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© Springer International Publishing AG, part of Springer Nature 2018

Authors and Affiliations

  1. 1.Department of PathologyJohns Hopkins University School of MedicineBaltimoreUSA
  2. 2.Department of Pathology and OncologyJohns Hopkins University School of MedicineBaltimoreUSA

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