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Updated: Mar 23, 2026
Author Spotlight: Unveiling Transmembrane Protein Family-Related Markers in Gastric Cancer and Implications for Targeted Therapies
Published on: September 15, 2023
Transcript level of AKR1C3 is down-regulated in gastric cancer
Bartosz Adam Frycz1, Dawid Murawa2,3, Maciej Borejsza-Wysocki4
1a Department of Biochemistry and Molecular Biology, University of Medical Sciences, Poznań, Poland.
Abstract:
Steroid hormones have been shown to play a role in gastric carcinogenesis. Large amounts of steroid hormones are locally produced in the peripheral tissues of both genders. Type 5 of 17β-hydroxysteroid dehydrogenase, encoded by the AKR1C3 gene, plays a pivotal role in both androgen and estrogen metabolism, and its expression was found to be deregulated in different cancers. In this study we measured AKR1C3 transcript and protein levels in nontumoral and primary tumoral gastric tissues, and evaluated their association with some clinicopathological features of gastric cancer (GC). We found decreased levels of AKR1C3 transcript (p < 0.0001) and protein (p = 0.0021) in GC tissues compared with the adjacent, apparently histopathologically normal, mucosa. Lower levels of AKR1C3 transcript were observed in diffuse and intestinal types of GC, whereas AKR1C3 protein levels were decreased in tumors with multisite localization, in diffuse histological type, T3, T4, and G3 grades. We also determined the effect of the histone deacetylase inhibitor sodium butyrate (NaBu) on AKR1C3 expression in EPG 85-257 and HGC-27 GC cell lines. We found that NaBu elevates the levels of both AKR1C3 transcript and protein in the cell lines we investigated. Together, our results suggest that decreased expression of AKR1C3 may be involved in development of GC and can be restored by NaBu.
Insights
Decreased expression of the AKR1C3 gene, crucial for steroid hormone metabolism, is linked to gastric cancer (GC) development. Sodium butyrate (NaBu) may restore AKR1C3 levels, offering a potential therapeutic avenue for GC.
Area of Science:
- Endocrinology
- Oncology
- Molecular Biology
Background:
- Steroid hormones influence gastric carcinogenesis.
- The AKR1C3 gene encodes 17β-hydroxysteroid dehydrogenase type 5, vital for androgen and estrogen metabolism.
- AKR1C3 expression is altered in various cancers.
Purpose of the Study:
- To investigate AKR1C3 transcript and protein levels in gastric cancer (GC) tissues.
- To correlate AKR1C3 expression with GC clinicopathological features.
- To assess the effect of sodium butyrate (NaBu) on AKR1C3 expression in GC cell lines.
Main Methods:
- Quantitative analysis of AKR1C3 transcript and protein in tumor and adjacent non-tumoral gastric tissues.
- Correlation analysis with clinicopathological parameters (histological type, tumor grade, localization).
- In vitro study using GC cell lines (EPG 85-257, HGC-27) treated with NaBu.
Main Results:
- Significantly decreased AKR1C3 transcript and protein levels were observed in GC tissues compared to normal mucosa.
- Lower AKR1C3 transcript levels correlated with diffuse and intestinal GC types.
- Reduced AKR1C3 protein levels were associated with multisite localization, diffuse type, advanced T and G grades.
- NaBu treatment increased both AKR1C3 transcript and protein levels in GC cell lines.
Conclusions:
- Downregulation of AKR1C3 expression is implicated in gastric cancer development.
- AKR1C3 expression can be modulated by NaBu, suggesting therapeutic potential.
- Targeting AKR1C3 may represent a novel strategy in gastric cancer treatment.
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