TY - CHAP
T1 - Targeting Metabolic Cross Talk Between Cancer Cells and Cancer-Associated Fibroblasts
AU - Jung, Jin Gyoung
AU - Le, Anne
N1 - Publisher Copyright:
© 2021, The Author(s).
PY - 2021
Y1 - 2021
N2 - Although cancer has classically been regarded as a genetic disease of uncontrolled cell growth, the importance of the tumor microenvironment (TME) [1, 2] is continuously emphasized by the accumulating evidence that cancer growth is not simply dependent on the cancer cells themselves [3, 4] but also dependent on angiogenesis [5–8], inflammation [9, 10], and the supporting roles of cancer-associated fibroblasts (CAFs) [11–13]. 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 [14], many studies have aimed to uncover the cross talk between cancer cells and CAFs. Moreover, a new paradigm in cancer metabolism shows how cancer cells act like “metabolic parasites” to take up the high-energy metabolites, such as lactate, ketone bodies, free fatty acids, and glutamine from supporting cells, including CAFs and cancer-associated adipocytes (CAAs) [15, 16]. This chapter provides an overview of the metabolic coupling between CAFs and cancer cells to further define the therapeutic options to disrupt the CAF-cancer cell interactions.
AB - Although cancer has classically been regarded as a genetic disease of uncontrolled cell growth, the importance of the tumor microenvironment (TME) [1, 2] is continuously emphasized by the accumulating evidence that cancer growth is not simply dependent on the cancer cells themselves [3, 4] but also dependent on angiogenesis [5–8], inflammation [9, 10], and the supporting roles of cancer-associated fibroblasts (CAFs) [11–13]. 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 [14], many studies have aimed to uncover the cross talk between cancer cells and CAFs. Moreover, a new paradigm in cancer metabolism shows how cancer cells act like “metabolic parasites” to take up the high-energy metabolites, such as lactate, ketone bodies, free fatty acids, and glutamine from supporting cells, including CAFs and cancer-associated adipocytes (CAAs) [15, 16]. This chapter provides an overview of the metabolic coupling between CAFs and cancer cells to further define the therapeutic options to disrupt the CAF-cancer cell interactions.
KW - Cancer therapy
KW - Cancer-associated adipocytes
KW - Cancer-associated fibroblasts
KW - Metabolism
KW - Metabolites
KW - Tumor microenvironment
UR - http://www.scopus.com/inward/record.url?scp=85106441810&partnerID=8YFLogxK
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U2 - 10.1007/978-3-030-65768-0_15
DO - 10.1007/978-3-030-65768-0_15
M3 - Chapter
C2 - 34014545
AN - SCOPUS:85106441810
T3 - Advances in Experimental Medicine and Biology
SP - 205
EP - 214
BT - Advances in Experimental Medicine and Biology
PB - Springer
ER -