Abstract
The Hippo pathway is highly conserved from Drosophila to mammals. As a key regulator of cell proliferation, the Hippo pathway controls tissue homeostasis and has a major impact on tumorigenesis. The originally defined core components of the Hippo pathway in mammals include STK3/4, LATS1/2, YAP1/TAZ, TEAD, VGLL4, and NF2. However, for most of these genes, mutations and copy number variations are relatively uncommon in human cancer. Several other recently identified upstream and downstream regulators of Hippo signaling, including FAT1, SHANK2, Gq/11, and SWI/SNF complex, are more commonly dysregulated in human cancer at the genomic level. This review will discuss major genomic events in human cancer that enable cancer cells to escape the tumor-suppressive effects of Hippo signaling.
Highlights
The Hippo signaling pathway is highly conserved through evolution
When the Hippo pathway is dysregulated, cells will acquire the potential for uncontrolled proliferation, promoting cancer formation
Mutations and/or copy number abnormalities directly impacting the core Hippo kinases are relatively rare in human cancers, cancer cells manage to escape from Hippo regulation by means of other upstream and downstream Hippo regulators, including FAT atypical cadherin 1 (FAT1), SHANK2, SWI/SNF, Gq/11, Vestigial-like family member4 (VGLL4), etc
Summary
The Hippo signaling pathway is highly conserved through evolution. The core components of the pathway were originally identified in Drosophila. Their orthologous genes in mammals were found later (Ma et al, 2019; Snigdha et al, 2019). A large number of studies have shown that the Hippo pathway controls organ size mainly by responding to cell contact and various mechanical signals. The Hippo pathway responds to cell polarity and G protein-coupled receptor (GPCR) signals. Gene dysregulation in human cancer can occur at various levels, including gene mutation/copy number abnormality, DNA methylation, over/under-expression, and posttranslational modifications. This review will focus on mutation and copy number abnormality of the Hippo pathway components in human cancers
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