ArticleOncology letters2017
mRNA expression of steroidogenic enzymes, steroid hormone receptors and their coregulators in gastric cancer.
Article in Oncology letters, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- ComprehensiveOncology reports · 2025Review
- Construction of a novel prognostic model for gastric cancer based on pharmacokinetics-related genes and comprehensive prognostic analysis.Frontiers in genetics · 2025Article
- Activation of endogenous glucocorticoids by HSD11B1 inhibits the antitumor immune response in renal cancer.Oncoimmunology · 2024Article
- Inhibition of NLRC5 attenuates the malignant growth and enhances the sensitivity of gastric cancer cells to 5-FU chemotherapy by blocking the carcinogenic effect of YY1.Experimental and therapeutic medicine · 2022Article
- MicroRNA profiles in five pairs of early gastric cancer tissues and adjacent non-cancerous tissues.Oncology letters · 2021Article
- Profiling of Steroid Metabolic Pathways in Human Plasma by GC-MS/MS Combined with Microwave-Assisted Derivatization for Diagnosis of Gastric Disorders.International journal of molecular sciences · 2021Article
- Preclinical evaluation of exemestane as a novel chemotherapy for gastric cancer.Journal of cellular and molecular medicine · 2019Article
- Comprehensive analysis of histone modification-associated genes on differential gene expression and prognosis in gastric cancer.Experimental and therapeutic medicine · 2019Article
- Gastric Normal Adjacent Mucosa Versus Healthy and Cancer Tissues: Distinctive Transcriptomic Profiles and Biological Features.Cancers · 2019Article
- Analysis of high risk factors for chronic atrophic gastritis.Saudi journal of gastroenterology : official journal of the Saudi Gastroenterology AssociationArticle
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epidemiological and experimental findings suggest that the development of gastric cancer (GC) is regulated by steroid hormones. In postmenopausal women and older men, the majority of steroid hormones are produced locally in peripheral tissue through the enzymatic conversion of steroid precursors. Therefore, using reverse transcription-quantitative polymerase chain reaction analysis, the mRNA expression of genes encoding steroidogenic enzymes, including steroid sulfatase (STS), hydroxy-delta-5-steroid dehydrogenase 3 beta- and steroid delta-isomerase 1 (HSD3B1), 17β-hydroxysteroid dehydrogenase type 7 and aromatase (CYP19A1), was investigated in primary tumoral and adjacent healthy gastric mucosa from 60 patients with GC. Furthermore, the mRNA levels for estrogen receptor α, estrogen receptor β (ESR2) and androgen receptor (AR), along with their coregulators, including proline, glutamate and leucine rich protein 1, CREB binding protein, nuclear receptor coactivator 1 (NCOA1), nuclear receptor corepressor 1 (NCOR1) and nuclear receptor subfamily 2 group F member 1 (NR2F1), were investigated. Additionally, the association between the mRNA expression of these genes and the clinicopathological features of patients with GC was examined. Significantly decreased levels of STS, HSD3B1, ESR2, AR, NCOA1 and NCOR1 mRNA, in addition to significantly increased levels of CYP19A1 mRNA were demonstrated in tumoral tissue samples compared with adjacent healthy gastric tissue samples. Deregulated expression of these genes in the analyzed tissue samples was associated with certain clinicopathological features of GC, such as age and localization of the tumor. The results of the current study suggest that all of the genes analyzed are expressed in tumoral and adjacent healthy gastric mucosa. In addition, the results indicate that abnormal expression of STS, ESR2, AR, NCOA1 and NCOR1 may serve a role in the development and progression of GC, and may be associated with specific clinicopathological features in patients with GC.
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