Genomics

Dataset Information

0

CD24 suppresses malignant phenotype by downregulation of SHH transcription through STAT1 inhibition in breast cancer cells [MCF-7]


ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE73959 | GEO | 2015/11/30

SECONDARY ACCESSION(S): PRJNA298589

REPOSITORIES: GEO

Similar Datasets

2015-11-30 | GSE73960 | GEO
| E-GEOD-17702 | biostudies-arrayexpress
2013-09-18 | GSE50950 | GEO
| E-GEOD-50950 | biostudies-arrayexpress
| E-GEOD-37702 | biostudies-arrayexpress
2010-06-03 | GSE17682 | GEO
| E-GEOD-36100 | biostudies-arrayexpress
| E-GEOD-42132 | biostudies-arrayexpress
2023-03-11 | PXD037275 | Pride
2023-03-31 | GSE201967 | GEO