<< Go Back

Metadata

Name
CD24 suppresses malignant phenotype by downregulation of SHH transcription through STAT1 inhibition in breast cancer cells [HCC1937]
Repository
Gene Expression Omnibus
Identifier
geo.series:GSE73960
Description
We describe a relationship between CD24 and the Hedgehog (Hh) ligand Sonic Hedgehog (SHH), and reveal a role for this relationship in the induction of a malignant phenotype in breast cancer. Anchorage-dependent proliferation, anchorage-independent proliferation, invasiveness, and tumorigenicity in breast cancer cells (BCCs) transfected with siRNA and plasmid targeting Hh signaling, CD24, and STAT1 were investigated. CD24 siRNA-transfected BCCs demonstrated higher expression of SHH and GLI1, increased anchorage-independent proliferation, enhanced invasiveness and superior tumorigenicity compared with control. Conversely, CD24 forced-expressing BCCs possessed decreased SHH and GLI1 expression, anchorage-independent proliferation, and invasiveness. Suppression of SHH decreased invasiveness through inhibition of matrix metalloproteinase (MMP)-2 expression, GLI1 expression, anchorage-independent proliferation, tumorigenicity, and tumor volume in vivo in CD24 siRNA-transfected BCCs. DNA microarray analysis identified STAT1 as a connection between CD24 and SHH. CD24 siRNA-transfected BCCs with concurrent STAT1 inhibition exhibited decreased SHH expression, invasiveness, anchorage-independent proliferation, tumorigenicity, and tumor volume in vivo. Consistently, STAT1 over-expression induced elevated SHH expression, invasiveness, and anchorage-independent proliferation in BCCs. These results suggest that CD24 suppresses development of a malignant phenotype by down-regulating SHH transcription through STAT1 inhibition.
Data or Study Types
Expression profiling by array
Source Organization
National Center for Biotechnology Information
Access Conditions
available
Year
2015
Access Hyperlink
http://www.ncbi.nlm.nih.gov/sites/GDSbrowser?acc=GSE73960

Distributions