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| Status |
Public on Nov 30, 2015 |
| Title |
CD24 suppresses malignant phenotype by downregulation of SHH transcription through STAT1 inhibition in breast cancer cells [HCC1937] |
| Organism |
Homo sapiens |
| Experiment type |
Expression profiling by array
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| 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.
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| 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.
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| Contributor(s) |
Suyama K, Onishi H, Imaizumi A, Shinkai K, Umebayashi M, Kubo M, Mizuuchi Y, Oda Y, Tanaka M, Nakamura M, Katano M |
| Citation missing |
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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
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| Organization name |
Graduate School of Medical Sciences, Kyushu University
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| Department |
Department of Cancer Therapy and Research
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| Street address |
3-1-1 Maidashi, Higashi-ku
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| City |
Fukuoka |
| ZIP/Postal code |
812-8582 |
| Country |
Japan |
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| Platforms (1) |
| GPL17077 |
Agilent-039494 SurePrint G3 Human GE v2 8x60K Microarray 039381 (Probe Name version) |
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| Samples (2) |
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| This SubSeries is part of SuperSeries: |
| GSE73961 |
CD24 suppresses malignant phenotype by downregulation of SHH transcription through STAT1 inhibition in breast cancer cells |
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| Relations |
| BioProject |
PRJNA298588 |
| Supplementary file |
Size |
Download |
File type/resource |
| GSE73960_RAW.tar |
24.6 Mb |
(http)(custom) |
TAR (of TXT) |
| Processed data included within Sample table |
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