ArticleEndocrine connections2017
Expression of renin-angiotensin system (RAS) components in endometrial cancer.
Article in Endocrine connections, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
36 citing papers in PubMed, 65 citations in OpenAlex.
- Characterization of elevated levels of endometrial renin-angiotensin system components suggest a role in endometrial repair.Frontiers in endocrinology · 2026Article
- Effects of Inhibitors of the Activity of the Circulating Renin-Angiotensin System on the Growth and Proliferation of Endometrial Cancer Cells.International journal of molecular sciences · 2025Article
- Angiotensin‑converting enzyme 2 expression in human tumors: Implications for prognosis and therapy (Review).Oncology reports · 2025Review
- Non-Hormonal Strategies in Endometriosis: Targets with Future Clinical Potential.Journal of clinical medicine · 2025Review
- The possible role furin and furin inhibitors in endometrial adenocarcinoma: A narrative review.Cancer reports (Hoboken, N.J.) · 2024Review
- Association between metabolic disorders and clinicopathologic features in endometrial cancer.Frontiers in endocrinology · 2024Article
- Article
- Elucidating the Role of Pro-renin Receptors in Pancreatic Ductal Adenocarcinoma Progression: A Novel Therapeutic Target in Cancer Therapy.Current cancer drug targets · 2024Review
- The renin-angiotensin-aldosterone system (RAAS) signaling pathways and cancer: foes versus allies.Cancer cell international · 2023Review
- A functional mechanism for a non-coding variant near AGTR2 associated with risk for preterm birth.BMC medicine · 2023Article
- Targeting the (pro)renin receptor in cancers: from signaling to pathophysiological effects.Journal of cancer research and clinical oncology · 2023Review
- COVID-19-The Shift of Homeostasis into Oncopathology or Chronic Fibrosis in Terms of Female Reproductive System Involvement.International journal of molecular sciences · 2023Review
- Screening of Differentially Expressed Genes Based on the ACRG Molecular Subtypes of Gastric Cancer and the Significance and Mechanism ofJournal of personalized medicine · 2023Article
- Renin-Angiotensin-Aldosterone System Inhibitors and Development of Gynecologic Cancers: A 23 Million Individual Population-Based Study.International journal of molecular sciences · 2023Article
- Unraveling the relationship between the renin-angiotensin system and endometrial cancer: a comprehensive review.Frontiers in oncology · 2023Review
- Progesterone differentially affects the transcriptomic profiles of cow endometrial cell types.BMC genomics · 2022Article
- Physiological and pathological roles of Ang II and Ang- (1-7) in the female reproductive system.Frontiers in endocrinology · 2022Review
- Role of the prorenin receptor in endometrial cancer cell growth.Oncotarget · 2022Article
- Serum soluble (pro)renin receptor level as a prognostic factor in patients undergoing maintenance hemodialysis.Scientific reports · 2021Article
- Canonical TGFβ Signaling and Its Contribution to Endometrial Cancer Development and Progression-Underestimated Target of Anticancer Strategies.Journal of clinical medicine · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A dysfunctional endometrial renin-angiotensin system (RAS) could aid the growth and spread of endometrial cancer. To determine if the RAS is altered in endometrial cancer, we measured RAS gene expression and protein levels in 30 human formalin-fixed, paraffin-embedded (FFPE) endometrioid carcinomas and their adjacent endometrium. All components of the RAS were expressed in most tumours and in adjacent endometrium; mRNA levels of (pro)renin receptor (ATP6AP2), angiotensin II type 1 receptor (AGTR1), angiotensin-converting enzyme (ACE1) and angiotensin-converting enzyme 2 (ACE2) mRNA levels were greater in tumour tissue than adjacent non-cancerous endometrium (P = 0.023, 0.008, 0.004 and 0.046, respectively). Prorenin, ATP6AP2, AGTR1, AGTR2 and ACE2 proteins were abundantly expressed in both cancerous and adjacent non-cancerous endometrium. Staining was most intense in cancerous glandular epithelium. One potential target of the endometrial RAS, transforming growth factor beta-1 (TGFB1), which is essential for epithelial-to-mesenchymal transition, was also upregulated in endometrial cancer tissue (P = 0.001). Interestingly, TGFB1 was strongly correlated with RAS expression and was upregulated in tumour tissue. This study is the first to characterise the mRNA and protein expression of all RAS components in cancerous and adjacent non-cancerous endometrium. The greater expression of ATP6AP2, AGTR1 and ACE1, key elements of the pro-angiogenic/proliferative arm of the RAS, suggests that the RAS plays a role in the growth and spread of endometrial cancer. Therefore, existing drugs that inhibit the RAS and which are used to treat hypertension may have potential as treatments for endometrial cancer.
Indexed as
Identifiers
What OpenQuestion holds
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.