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Updated: Oct 15, 2026

The Soft Agar Colony Formation Assay
Published on: October 27, 2014
Isolation and characterization of a novel human gene, DRCTNNB1A, the expression of which is down-regulated by
T Kawasoe1, Y Furukawa, Y Daigo
1Laboratory of Molecular Medicine, Human Genome Center, Institute of Medical Science, The University of Tokyo, Japan.
Abstract:
Beta-catenin plays significant roles in cell-to-cell adhesion and the Wnt/Wg signal transduction pathway. Accumulation of this protein in the cytoplasm and nucleus as a result of mutations of the adenomatous polyposis coli tumor suppressor gene or of the beta-catenin gene itself is often seen in a wide variety of tumors including carcinomas of the colon, liver, uterus, and brain. Interaction of accumulated beta-catenin with Tcf/Lef transcription factors is known to deregulate expression of some downstream genes, but the precise mechanisms whereby beta-catenin contributes to carcinogenesis remain to be disclosed. Here we report isolation of a novel murine gene, Drctnnb1a (down-regulated by Ctnnb1, a), the expression of which was experimentally down-regulated in response to the activated form of beta-catenin. To investigate a possible role of DRCTNNB1A in cancers, we also isolated the human homologue, DRCTNNB1A, the deduced product of which was 91% identical to the murine protein. The transcript was expressed in all human tissues examined, and we assigned the genomic location of DRCTNNB1A to chromosomal band 7p15.3 by in situ hybridization. Expression of DRCTNNB1A in SW480 colon cancer cells was significantly increased in response to reduction of intracellular beta-catenin by adenovirus-mediated transfer of the beta-catenin-binding domain of the adenomatous polyposis coli gene into the cells. Furthermore, we documented reduced expression of DRCTNNB1A in 12 of 15 primary colorectal cancers examined, compared with corresponding adjacent noncancerous mucosae. Our results implied that DRCTNNB1A is one of the genes involved in the beta-catenin-Tcf/Lef signaling pathway, and that reduced expression of DRCTNNB1A may have some role in colorectal carcinogenesis.
Insights
Researchers identified a new gene, DRCTNNB1A, involved in the beta-catenin signaling pathway. Reduced expression of DRCTNNB1A was observed in colorectal cancers, suggesting its role in carcinogenesis.
Area of Science:
- Molecular Biology
- Cancer Research
- Genetics
Background:
- Beta-catenin is crucial for cell adhesion and Wnt signaling.
- Accumulated beta-catenin, due to mutations, is linked to various cancers.
- The exact role of beta-catenin in carcinogenesis is not fully understood.
Purpose of the Study:
- To identify novel genes regulated by beta-catenin.
- To investigate the role of the identified gene, DRCTNNB1A, in cancer, particularly colorectal cancer.
Main Methods:
- Isolation and characterization of murine and human DRCTNNB1A.
- In situ hybridization to determine genomic location.
- Adenovirus-mediated gene transfer to modulate beta-catenin levels in colon cancer cells.
- Quantitative analysis of DRCTNNB1A expression in primary colorectal cancers.
Main Results:
- A novel gene, DRCTNNB1A, was identified and found to be down-regulated by activated beta-catenin.
- Human DRCTNNB1A shares 91% identity with its murine counterpart and is expressed in all examined tissues.
- DRCTNNB1A expression increased upon reduction of intracellular beta-catenin in colon cancer cells.
- Reduced DRCTNNB1A expression was found in a majority of primary colorectal cancers.
Conclusions:
- DRCTNNB1A is implicated as a gene within the beta-catenin-Tcf/Lef signaling pathway.
- Down-regulation of DRCTNNB1A may contribute to the development of colorectal cancer.
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