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• W2182198647 abstract "Deregulated Hedgehog (HH)/GLI signaling plays an etiologic role in the initiation, progression and maintenance of many cancers. Small molecule targeting of HH signaling by inhibiting the essential pathway effector Smoothened (SMO) has proven exceptionally efficient for the treatment of advanced and metastatic basal cell carcinoma. That said, severe side effects, limited response rates, SMO-independent GLI signaling and rapid development of drug resistance limit the therapeutic success of SMO antagonists, urgently calling for the identification of alternative and additional strategies repressing oncogenic HH signaling. In this perspective article we highlight recent findings showing that the Toll-like receptor-7/8 (TLR7/8) agonist imiquimod (IMQ), an immune modulator approved for the treatment of basal cell carcinoma, can also act as a potent cell autonomous inhibitor of oncogenic HH signaling. Surprisingly, IMQ reduces HH signal strength independent of TLR signaling, via adenosine receptor (ADORA)/Adenylate cyclase (AC)/Protein kinase A (PKA) activation. We here highlight the molecular mechanisms of IMQ-mediated repression of HH/GLI and discuss the possible benefits as well as challenges of using ADORA agonists for the treatment of HH-associated cancer." @default.
• W2182198647 created "2016-06-24" @default.
• W2182198647 creator A5016585570 @default.
• W2182198647 creator A5037111326 @default.
• W2182198647 creator A5091197265 @default.
• W2182198647 date "2014-09-16" @default.
• W2182198647 modified "2023-10-18" @default.
• W2182198647 title "An old friend with new skills: Imiquimod as novel inhibitor of Hedgehog signaling in basal cell carcinoma" @default.
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• W2182198647 doi "https://doi.org/10.18632/oncoscience.80" @default.
• W2182198647 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4278338" @default.
• W2182198647 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25594066" @default.
• W2182198647 hasPublicationYear "2014" @default.
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