ABI3 ectopic expression reduces in vitro and in vivocell growth properties while inducing senescence
Open accessAbstract
Background: Mounting evidence has indicated that ABI3 (ABI family member 3) function as a tumor suppressor gene, although the molecular mechanism by which ABI3 acts remains largely unknown. Methods: The present study investigated ABI3 expression in a large panel of benign and malignant thyroid tumors and explored a correlation between the expression of ABI3 and its potential partner ABI3-binding protein (ABI3BP). We next explored the biological effects of ABI3 ectopic expression in thyroid and colon carcinoma cell lines, in which its expression was reduced or absent. Results: We not only observed that ABI3 expression is reduced or lost in most carcinomas but also that there is a positive correlation between ABI3 and ABI3BP expression. Ectopic expression of ABI3 was sufficient to lead to a lower transforming activity, reduced tumor in vitro growth properties, suppressed in vitro anchorage-independent growth and in vivo tumor formation while, cellular senescence increased. These responses were accompanied by the up-regulation of the cell cycle inhibitor p21 WAF1 and reduced ERK phosphorylation and E2F1 expression. Conclusions: Our result links ABI3 to the pathogenesis and progression of some cancers and suggests that ABI3 or its pathway might have interest as therapeutic target. These results also suggest that the pathways through which ABI3 works should be further characterized.
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Forced expression of ABI3 in v-src-transformed NIH3T3 (SRD) cells, thyroid cancer cells, or colon cancer cells inhibits cell growth, invasiveness and migration, and enhances cellular senescence in vitro and reduces the tumor growth and metastasis in vivo, indicating that ABI3 acts as a tumor suppressor gene.
“Forced expression of ABI3 in v-src-transformed NIH3T3 (SRD) cells, thyroid cancer cells, or colon cancer cells inhibits cell growth, invasiveness and migration, and enhances cellular senescence in vitro and reduces the tumor growth and metastasis in vivo, indicating that ABI3 acts as a tumor suppressor gene (20,22).”
From Microglia express ABI3 in the brains of Alzheimer's disease and Nasu-Hakola disease (2017) · cites this paper as [22]
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Karahan, H., Smith, D. C., Kim, B., Dabin, L. C., Al-Amin, M. M., Wijeratne, H. R. S., Pennington, T., Viana di Prisco, G., McCord, B., Lin, P. B.-C., et al. (2021) · Science Advances · doi:10.1126/sciadv.abe3954 · Cited by 53 · see citing works
Microglia express ABI3 in the brains of Alzheimer's disease and Nasu-Hakola disease
Satoh, J.-I., Kino, Y., Yanaizu, M., Tosaki, Y., Sakai, K., Ishida, T., & Saito, Y. (2017) · Intractable & Rare Diseases Research · doi:10.5582/irdr.2017.01073 · Cited by 55 · see citing works
- Authors
- Latini, F. R., Hemerly, J. P., Freitas, B. C., Oler, G., Riggins, G. J., & Cerutti, J. M.
- Affiliations
- Universidade Federal de São Paulo (BR)
- Johns Hopkins University (US)
- Corresponding author
- Cerutti, Janete M
- Venue
- BMC Cancer
- Published
- 2011-01-11
- Volume
- 11
- Issue
- 1
- Pages
- 11-11
- ISSN
- 1471-2407 (ISSN-L)
- PMC
- PMC3032749
- OpenAlex
- W2071625408
- Cited by
- 48
- References
- 2
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 4 · 2023: 5 · 2022: 2 · 2021: 4 · 2020: 5 · 2019: 4 · 2017: 5 · 2016: 4 · 2015: 2 · 2014: 1 · 2013: 3 · 2012: 5
- FWCI
- 1.34
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- BMC Cancer (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Americanae (AECID Library) (submittedVersion, other-oa)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (submittedVersion, other-oa)
- Funders
- Fundação de Amparo à Pesquisa do Estado de São Paulo (05/60330-8, 04/15288-0)
- Conselho Nacional de Desenvolvimento Científico e Tecnológico
- National Institutes of Health
- National Cancer Institute (CA113461)
- Topics
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Cancer Diagnosis and Treatment
- Keywords
- ABI3, tumor suppressor, ectopic expression, cellular senescence, anchorage-independent growth, tumor growth, thyroid cancer, colon cancer, p21, ERK1/2 phosphorylation, E2F1, cell cycle inhibition, therapeutic target
- MeSH terms
- Animals, Carrier Proteins, Cell Cycle, Cell Survival, Humans, Male, Mice, Nude, Neoplasms, Experimental, Phosphorylation, Thyroid Neoplasms, Transplantation, Heterologous, Blotting, Western, Gene Expression Regulation, Neoplastic, Cellular Senescence, Apoptosis, HT29 Cells, Reverse Transcriptase Polymerase Chain Reaction, Cell Line, Tumor, Tumor Burden, Extracellular Signal-Regulated MAP Kinases, Adaptor Proteins, Signal Transducing, Cell Proliferation, E2F1 Transcription Factor, Cyclin-Dependent Kinase Inhibitor p21, Mice
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