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Series GSE73959 Query DataSets for GSE73959
Status Public on Nov 30, 2015
Title CD24 suppresses malignant phenotype by downregulation of SHH transcription through STAT1 inhibition in breast cancer cells [MCF-7]
Organism Homo sapiens
Experiment type Expression profiling by array
Summary 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.
 
Overall design We focus on the BCSC marker CD24, and the Hh ligand SHH, and reveal a role for these molecules in the induction of a malignant phenotype in breast cancer.
 
Contributor(s) Suyama K, Onishi H, Imaizumi A, Shinkai K, Umebayashi M, Kubo M, Mizuuchi Y, Oda Y, Tanaka M, Nakamura M, Katano M
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Submission date Oct 13, 2015
Last update date Apr 23, 2018
Contact name Hideya Onishi
E-mail(s) ohnishi@surg1.med.kyushu-u.ac.jp
Organization name Graduate School of Medical Sciences, Kyushu University
Department Department of Cancer Therapy and Research
Street address 3-1-1 Maidashi, Higashi-ku
City Fukuoka
ZIP/Postal code 812-8582
Country Japan
 
Platforms (1)
GPL17077 Agilent-039494 SurePrint G3 Human GE v2 8x60K Microarray 039381 (Probe Name version)
Samples (2)
GSM1906776 Control siRNA-treated MCF-7 cells
GSM1906777 CD24 siRNA-treated MCF-7 cells
This SubSeries is part of SuperSeries:
GSE73961 CD24 suppresses malignant phenotype by downregulation of SHH transcription through STAT1 inhibition in breast cancer cells
Relations
BioProject PRJNA298589

Download family Format
SOFT formatted family file(s) SOFTHelp
MINiML formatted family file(s) MINiMLHelp
Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE73959_RAW.tar 24.5 Mb (http)(custom) TAR (of TXT)
Processed data included within Sample table

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