ArticleOncology letters2020
Frequent promoter methylation of HOXD10 in endometrial carcinoma and its pathological significance.
Article in Oncology letters, 2020. 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, 12 citations in OpenAlex.
- Review
- DNA-mediated ZNF649 downregulation modulates the Hedgehog signaling pathway to reduce the sensitivity of gastric cardia cancer to 5-FU.Journal of clinical biochemistry and nutrition · 2026Article
- HOXD10 attenuates renal fibrosis by inhibiting NOX4-induced ferroptosis.Cell death & disease · 2024Article
- Gastrodin Induces Ferroptosis of Glioma Cells via Upregulation of Homeobox D10.Molecules (Basel, Switzerland) · 2023Article
- Integrative multi-omic cancer profiling reveals DNA methylation patterns associated with therapeutic vulnerability and cell-of-origin.Cancer cell · 2023Article
- MiR-501 promotes tumor proliferation and metastasis by targeting HOXD10 in endometrial cancer.Cellular & molecular biology letters · 2021Article
- Article
- RestoringFrontiers in oncology · 2021Article
- Data mining analysis of the prognostic impact of NJournal of Cancer · 2021Article
- The Role of MicroRNAs in Development of Endometrial Cancer: A Literature Review.Journal of reproduction & infertilityReview
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Homeobox D 10 (HOXD10) is important in cell differentiation and morphogenesis and serves as a tumor suppressor gene (TSG) in a number of malignancies. The present study investigated its promoter methylation status and association with the clinicopathological features of endometrial cancer (EC), and measured HOXD10 protein expression levels. EC samples (n=62), including 50 endometroid adenocarcinoma (EA) and 12 mucinous endometrial carcinoma samples (EC) and 70 non-cancerous samples were collected. All samples were evaluated for the methylation status of several TSGs, including HOXD10, using methylation-specific PCR. HOXD10 expression level was evaluated using immunohistochemistry. 5-Aza-2-deoxycytidine treatment was performed in the EC cell line Ishikawa to observe the change in HOXD10 expression levels. HOXD10 promoter methylation was more frequent in cancer samples (P<0.001). Downregulation of HOXD10 in EC samples was confirmed at the protein level using immunohistochemistry (P<0.001) and immunohistochemical staining was negatively associated with methylation status (P<0.05). Less HOXD10 protein was expressed in MEC compared with EA samples (P<0.001). The HOXD10 promoter was hypermethylated in both EA and MEC, causing decreased HOXD10 protein expression levels in EC cells. HOXD10 expression levels were partially reversed by 5-Aza-2-deoxycytidine treatment. The results of the present study demonstrated that epigenetic silencing of HOXD10 putatively contributed to the tumorigenesis of EA. Although there was no significant difference in HOXD10 methylation between EA and MEC, HOXD10 protein expression levels differed between these two diseases, indicating that it may be a useful protein biomarker for distinguishing between these two lesions.
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