TY - JOUR
T1 - ERBB Signaling Pathway in Cancer Stem Cells
AU - Hassan, Ghmkin
AU - Seno, Masaharu
N1 - Publisher Copyright:
© 2022. The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Nature Switzerland AG.
PY - 2022
Y1 - 2022
N2 - The epidermal growth factor receptor (EGFR) was first tyrosine kinase receptor linked to human cancers. EGFR or ERBB1 is a member of ERBB subfamily, which consists of four type I transmembrane receptor tyrosine kinases, ERBB1, 2, 3 and 4. ERBBs form homo/heterodimers after ligand binding except ERBB2 and consequently becomes activated. Different signal pathways, such as phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT), RAS/RAF/MEK/ERK, phospholipase Cγ and JAK-STAT, are triggered by ERBB activation. Since ERBBs, through these pathways, regulate stemness and differentiation of cancer stem cells (CSCs), their roles in CSC tumorigenicity have extensively been investigated. The hyperactivation of ERBBs and its downstream pathways stimulated by either genetic and/or epigenetic factors are frequently described in many types of human cancers. Their dysregulations make cells acquiring CSC characters such as survival, tumorigenicity and stemness. Because of the roles in tumor growth and progress, ERBBs are considered to be one of the drug targets as cancer treatment strategy. In this chapter, we will summarize the structure, function and roles of ERBB subfamily along with their relative pathways regulating the stemness and tumorigenicity of CSCs. Finally, we will discuss the targeting therapy strategies of cancer along with ERBBs in addition to some challenges and future perspectives.
AB - The epidermal growth factor receptor (EGFR) was first tyrosine kinase receptor linked to human cancers. EGFR or ERBB1 is a member of ERBB subfamily, which consists of four type I transmembrane receptor tyrosine kinases, ERBB1, 2, 3 and 4. ERBBs form homo/heterodimers after ligand binding except ERBB2 and consequently becomes activated. Different signal pathways, such as phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT), RAS/RAF/MEK/ERK, phospholipase Cγ and JAK-STAT, are triggered by ERBB activation. Since ERBBs, through these pathways, regulate stemness and differentiation of cancer stem cells (CSCs), their roles in CSC tumorigenicity have extensively been investigated. The hyperactivation of ERBBs and its downstream pathways stimulated by either genetic and/or epigenetic factors are frequently described in many types of human cancers. Their dysregulations make cells acquiring CSC characters such as survival, tumorigenicity and stemness. Because of the roles in tumor growth and progress, ERBBs are considered to be one of the drug targets as cancer treatment strategy. In this chapter, we will summarize the structure, function and roles of ERBB subfamily along with their relative pathways regulating the stemness and tumorigenicity of CSCs. Finally, we will discuss the targeting therapy strategies of cancer along with ERBBs in addition to some challenges and future perspectives.
KW - Cancer stem cells
KW - Cancer treatment
KW - EGF
KW - ERBBs
KW - HER2
KW - Signal pathways
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U2 - 10.1007/978-3-031-12974-2_3
DO - 10.1007/978-3-031-12974-2_3
M3 - Article
C2 - 36587302
AN - SCOPUS:85145425758
SN - 0065-2598
VL - 1393
SP - 65
EP - 81
JO - Advances in experimental medicine and biology
JF - Advances in experimental medicine and biology
ER -
