Abstract:
:Molecularly defined subclassification is associated with phenotypic malignancy of glioblastoma (GBM). However, current understanding of the molecular basis of subclass conversion that is often involved in GBM recurrence remain rudimentary at best. Here we report that canonical Wnt signalling that is active in proneural (PN) but inactive in mesenchymal (MES) GBM, along with miR-125b and miR-20b that are expressed at high levels in PN compared with MES GBM, comprise a regulatory circuit involving TCF4-miR-125b/miR-20b-FZD6. FZD6 acts as a negative regulator of this circuit by activating CaMKII-TAK1-NLK signalling, which, in turn, attenuates Wnt pathway activity while promoting STAT3 and NF-κB signalling that are important regulators of the MES-associated phenotype. These findings are confirmed by targeting differentially enriched pathways in PN versus MES GBM that results in inhibition of distinct GBM subtypes. Correlative expressions of the components of this circuit are prognostic relevant for clinical GBM. Our findings provide insights for understanding GBM pathogenesis and for improving treatment of GBM.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Huang T,Alvarez AA,Pangeni RP,Horbinski CM,Lu S,Kim SH,James CD,J Raizer J,A Kessler J,Brenann CW,Sulman EP,Finocchiaro G,Tan M,Nishikawa R,Lu X,Nakano I,Hu B,Cheng SYdoi
10.1038/ncomms12885subject
Has Abstractpub_date
2016-10-04 00:00:00pages
12885issn
2041-1723pii
ncomms12885journal_volume
7pub_type
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