Abstract | BACKGROUND & AIMS: METHODS: RESULTS: TOPK was shown to promote transformation in vitro and in vivo, and knockdown of TOPK in HCT116 colorectal cancer cells reduced this cell lines' tumorigenic properties in vitro and in vivo. Furthermore, a positive feedback loop between TOPK and ERK2 was identified. With epidermal growth factor treatment, knockdown of either TOPK or ERK2 in HCT116 cells resulted in a decreased phosphorylation of ERK2 or TOPK, respectively, and knockdown of TOPK in HCT116 colorectal cancer cells blocked the phosphorylation of downstream substrates of ERK2. CONCLUSIONS:
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Authors | Feng Zhu, Tatyana A Zykova, Bong Seok Kang, Zhe Wang, Mara C Ebeling, Yasuhito Abe, Wei-Ya Ma, Ann M Bode, Zigang Dong |
Journal | Gastroenterology
(Gastroenterology)
Vol. 133
Issue 1
Pg. 219-31
(Jul 2007)
ISSN: 0016-5085 [Print] United States |
PMID | 17631144
(Publication Type: Journal Article, Research Support, N.I.H., Extramural)
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Chemical References |
- Protein Serine-Threonine Kinases
- Mitogen-Activated Protein Kinase 1
- Mitogen-Activated Protein Kinase Kinases
- PDZ-binding kinase
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Topics |
- Amino Acid Sequence
- Animals
- Cell Transformation, Neoplastic
- Colonic Neoplasms
(metabolism, pathology)
- Enzyme Activation
- Epidermis
(metabolism, pathology)
- Feedback, Physiological
- Gene Expression Regulation, Enzymologic
- Gene Expression Regulation, Neoplastic
- HCT116 Cells
- Humans
- MAP Kinase Signaling System
(physiology)
- Mice
- Mice, Inbred BALB C
- Mice, Nude
- Mitogen-Activated Protein Kinase 1
(genetics, metabolism)
- Mitogen-Activated Protein Kinase Kinases
- Molecular Sequence Data
- Phosphorylation
- Protein Serine-Threonine Kinases
(genetics, metabolism)
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