ArticleTechnology in cancer research & treatment
High SENP3 Expression Promotes Cell Migration, Invasion, and Proliferation by Modulating DNA Methylation of E-Cadherin in Osteosarcoma.
Article in Technology in cancer research & treatment. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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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.
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- SENP1 regulates the malignant activities of osteosarcoma cells and antitumor immunity via the cGAS-STING signaling.Molecular and cellular biochemistry · 2026Article
- The SUMO specific peptidase SENP3 promotes papillary thyroid cancer progression by deSUMOylation of SETDB1 and regulating GLI2 transcription.Clinical and experimental medicine · 2026Article
- The SUMOylation and ubiquitination crosstalk in cancer.Journal of cancer research and clinical oncology · 2023Review
- Review
- Regulation of the Epithelial to Mesenchymal Transition in Osteosarcoma.Biomolecules · 2023Review
- Cancer-Associated Dysregulation of Sumo Regulators: Proteases and Ligases.International journal of molecular sciences · 2022Review
- SENP3 promotes tumor progression and is a novel prognostic biomarker in triple-negative breast cancer.Frontiers in oncology · 2022Article
- Integral Analyses of Competing Endogenous RNA Mechanisms and DNA Methylation Reveal Regulatory Mechanisms in Osteosarcoma.Frontiers in cell and developmental biology · 2021Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
SENP3, a sentrin/SUMO2/3-specific protease, is recognized as a transcriptional factor that accumulates under cellular oxidative stress and plays a significant role in the removal of SUMO2/3 modification. In our study, we examined a TCGA dataset and found that the transcripts per million (TPM) value of SENP3 is high in sarcoma, including osteosarcoma (OS). We found that SENP3 was highly expressed in OS cancer tissues when compared with osteofibrous dysplasia tissues. The survival data of SENP3 in TCGA showed that the sarcoma patients with higher SENP3 expression levels showed poor prognosis. In vitro, SENP3 knockdown in OS cancer cells inhibited cell proliferation, migration, and invasion and induced apoptosis. In contrast, SENP3 overexpression reversed these effects. Next, we found that SENP3 inhibited the expression of E-cadherin (E-Cad) by increasing methylation of the E-Cad promoter. Finally, E-Cad expression was increased in the OS cell line MG63 following methylation, and the cell proliferation, migration, and invasion capacity were decreased. In summary, SENP3 played a significant role in OS carcinogenesis and may act as a potential biomarker in the diagnosis and treatment of OS.
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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.