ArticleOncogene1999
Altered phenotype of HT29 colonic adenocarcinoma cells following expression of the DCC gene.
Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed, 31 citations in OpenAlex.
- Dependence and Guidance Receptors-DCC and Neogenin-In Partial EMT and the Actions of Serine Proteases.Frontiers in oncology · 2020Review
- Serine protease modulation of Dependence Receptors and EMT protein expression.Cancer biology & therapy · 2019Article
- Article
- Deleted in Colorectal Cancer (DCC) pathfinding: axon guidance gene finally turned tumor suppressor.Current drug targets · 2012Article
- Review
- Colorectal carcinogenesis: Review of human and experimental animal studies.Journal of carcinogenesis · 2009Article
- Role of netrin-1 and netrin-1 dependence receptors in colorectal cancers.British journal of cancer · 2005Review
- Dependence receptors: between life and death.Cellular and molecular life sciences : CMLS · 2004Review
- Mouse models for colorectal cancer.Oncogene · 1999Review
- Mutation and expression of the DCC gene in human lung cancer.Neoplasia (New York, N.Y.)Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
On 18q, frequently deleted in late stage colorectal cancers, a gene, Deleted in Colon Cancer (DCC), has been identified and postulated to play a role as a tumor suppressor gene. DCC is retained in the majority of mucinous tumors, which produce high levels of mucins, and seems to be preferentially expressed in intestinal goblet cells. To investigate whether DCC is related to mucin expression and can modulate the transformed phenotype, we introduced a full-length DCC cDNA into HT29 cells, which can be induced in vitro to express MUC2, the gene that encodes the major colonic mucin. Expression of DCC did not modulate constitutive or induced expression of MUC2, nor did DCC induce a mature goblet cell phenotype. However, HT29 clones expressing high and low levels of DCC protein showed a significant decrease in cell proliferation and tumorigenicity. Furthermore, increased shedding and an elevated rate of spontaneous apoptosis were associated with higher levels of expression of DCC. In summary, while restoration of DCC expression in a human colon carcinoma cell line did not influence expression of differentiation markers, DCC expression did affect the growth and tumorigenic properties of the cells suggesting that DCC can modulate the malignant phenotype of colon cancer.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.