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Estrogen-responsive RING finger mRNA induction in gastrointestinal carcinoma cells following bile acid treatment
B Jung1, T Vogt, F Mathieu-Daudé
1Sidney Kimmel Cancer Center, San Diego, CA 92121, USA.
Abstract:
The underlying molecular mechanisms of the tumor-promoting activity of bile acids such as chenodeoxycholic acid (CDCA) and deoxycholic acid (DCA) and the protective effect of ursodeoxycholic acid (UDCA) remain largely unclear. Using RNA arbitrarily primed PCR (RAP-PCR) for differential display, we identified, cloned and sequenced differentially expressed transcripts after treating gastric carcinoma cells (St 23132) with the bile acids CDCA, DCA and UDCA. One of these transcripts was identified to be an estrogen-responsive RING finger protein (efp) mRNA. The differential expression of efp in gastric cancer cells was confirmed by low stringency RT-PCR. efp mRNA levels were induced 3-fold in gastric carcinoma cells after CDCA and DCA treatment, whereas no change in expression was detected after UDCA treatment. Finally, treatment of the colon carcinoma cell line HT 29 with DCA resulted in a 2- to 5-fold induction of efp mRNA levels whereas UDCA did not induce efp. As expected, efp expression was also increased after 24 h of estrogen treatment. In summary, a synergy or a common pathway of tumor enhancement of bile acids and estrogen via efp in gastrointestinal carcinogenesis can be envisioned.
Insights
Tumor-promoting bile acids like chenodeoxycholic acid (CDCA) and deoxycholic acid (DCA) increase estrogen-responsive RING finger protein (efp) mRNA in gastric and colon cancer cells. Ursodeoxycholic acid (UDCA) did not affect efp levels.
Area of Science:
- Gastroenterology
- Molecular Biology
- Oncology
Background:
- Bile acids (CDCA, DCA, UDCA) play roles in gastrointestinal carcinogenesis, but their molecular mechanisms are unclear.
- Estrogen's role in gastrointestinal cancers is also being investigated.
- Understanding these interactions is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the molecular mechanisms of tumor-promoting bile acids (CDCA, DCA) and the protective effects of UDCA.
- To identify differentially expressed genes in gastric cancer cells treated with these bile acids.
- To explore the potential link between bile acids, estrogen, and gastrointestinal carcinogenesis.
Main Methods:
- Differential gene expression analysis using RNA arbitrarily primed PCR (RAP-PCR).
- Cloning and sequencing of differentially expressed transcripts.
- Confirmation of gene expression using low-stringency RT-PCR.
- Treatment of gastric and colon carcinoma cell lines with bile acids and estrogen.
Main Results:
- Identified and cloned an estrogen-responsive RING finger protein (efp) mRNA transcript.
- CDCA and DCA treatment induced efp mRNA levels 3-fold in gastric cancer cells.
- DCA treatment induced efp mRNA levels 2- to 5-fold in colon cancer cells; UDCA had no effect.
- Estrogen treatment also increased efp expression, suggesting a common pathway.
Conclusions:
- Bile acids (CDCA, DCA) can induce efp expression, similar to estrogen.
- A potential synergistic or common pathway involving bile acids, estrogen, and efp in gastrointestinal carcinogenesis is proposed.
- Further research is warranted to elucidate the role of efp in bile acid- and estrogen-mediated tumor promotion.
