PAX2 protein induces expression of cyclin D1 through activating AP-1 protein and promotes proliferation of colon cancer cells
Open accessAbstract
Paired box (PAX) 2, a transcription factor, plays a critical role in embryogenesis. When aberrantly expressed in adult tissues, it generally exhibits oncogenic properties. However, the underlying mechanisms remain unclear. We reported previously that the expression of PAX2 was up-regulated in human colon cancers. However, the role of PAX2 in colon cancer cells has yet to be determined. The aim of this study is to determine the function of PAX2 in colon cancer cells and to investigate the possible mechanisms underlain. We find that knockdown of PAX2 inhibits proliferation and xenograft growth of colon cancer cells. Inhibition of PAX2 results in a decreased expression of cyclin D1. Expression of cyclin D1 is found increased in human primary colon malignant tumors, and its expression is associated with that of PAX2. These data indicate that PAX2 is a positive regulator of expression of cyclin D1. We find that knockdown of PAX2 inhibits the activity of AP-1, a transcription factor that induces cyclin D1 expression, implying that PAX2 induces cyclin D1 through AP-1. PAX2 has little effect on expression of AP-1 members including c-Jun, c-Fos, and JunB. Our data show that PAX2 prevents JunB from binding c-Jun and enhances phosphorylation of c-Jun, which may elevate the activity of AP-1. Taken together, these results suggest that PAX2 promotes proliferation of colon cancer cells through AP-1.
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Transcription of genes such as cyclin D1 having NF-κB-binding sites, but not attenuated by PDCD4, may be predominantly regulated by other transcription factors or by other NF-κB proteins.
“Transcription of genes such as cyclin D1 having NF-κB-binding sites, but not attenuated by PDCD4, may be predominantly regulated by other transcription factors as described by others (41) or by other NF-κB proteins.”
From Tumor suppressor PDCD4 inhibits NF-κB-dependent transcription in human glioblastoma cells by direct interaction with p65 (2014) · cites this paper as [41]
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- Shtutman, M., Zhurinsky, J., Simcha, I., Albanese, C., D'Amico, M., Pestell, R., and Ben-Ze'ev, A. (1999) The cyclin D1 gene is a target of the -catenin/LEF-1 pathway. Proc. Natl. Acad. Sci. U.S.A. 96, 5522-5527
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Hwang, S.-K., Baker, A. R., Young, M. R., & Colburn, N. H. (2014) · Carcinogenesis · doi:10.1093/carcin/bgu008 · Cited by 49 · see citing works
- Authors
- Zhang, H.-S., Yan, B., Li, X.-B., Fan, L., Zhang, Y.-F., Wu, G.-H., Li, M., & Fang, J.
- Affiliations
- Chinese Academy of Sciences (CN)
- The University of Texas Health Science Center at Houston (US)
- Corresponding author
- Fang, Jing
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2012-12
- Volume
- 287
- Issue
- 53
- Pages
- 44164-44172
- ISSN
- 0021-9258 (ISSN-L)
- PMC
- PMC3531732
- OpenAlex
- W2092933936
- Cited by
- 32
- References
- 0
- Citations by year
- 2025: 1 · 2024: 3 · 2023: 1 · 2022: 2 · 2021: 3 · 2020: 1 · 2019: 2 · 2018: 3 · 2017: 2 · 2016: 5 · 2015: 3 · 2014: 4 · 2013: 2
- FWCI
- 1.42
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (30970586)
- Chinese Academy of Sciences
- Directorate for Biological Sciences
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
- Health Sciences › Medicine › Pathology and Forensic Medicine › Cancer Mechanisms and Therapy
- Keywords
- PAX2, cyclin D1, AP-1, colon cancer, cell proliferation, transcriptional regulation, c-Jun phosphorylation, JunB, c-fos, oncogenic transcription factor, xenograft tumor growth
- MeSH terms
- Animals, Colonic Neoplasms, Humans, Male, Mice, Inbred BALB C, Mice, Nude, Up-Regulation, Proto-Oncogene Proteins c-jun, Proto-Oncogene Proteins c-fos, Transcription Factor AP-1, Cyclin D1, Cell Line, Tumor, Cell Proliferation, Mice, PAX2 Transcription Factor
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