Glioma-associated oncogenes (GLIs) are zinc finger protein family members and downstream
regulatory factors of the classic Hedgehog (Hh) signaling pathway. GLI proteins influence
the growth and development of organisms and aid in tissue repair. However, aberrant expression of
the GLI family member GLI1 promotes carcinogenesis by inducing epithelial–mesenchymal transition
(EMT), angiogenesis, and other signaling pathways. Overexpression of GLI1 is thought to be
an indicator of poor prognosis as well as a potential therapeutic target for cancers. GLI inhibitors
such as zerumbone, GANT61, resveratrol, and cyclopamine depress the Hh pathway in vitro and in
vivo cancer research, and other non-canonical pathways may also activate expression of GLI1. Here,
we summarize GLI function in carcinogenesis and cancer-targeted therapy.
Keywords: Hedgehog signaling, GLI proteins, carcinogenesis, targeted therapy, non-canonical pathways, mutation.
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