ArticleOncotarget2014
De-SUMOylation of FOXC2 by SENP3 promotes the epithelial-mesenchymal transition in gastric cancer cells.
Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 60 citations in OpenAlex.
- Epigenetic alterations in cancer metastasis: molecular mechanisms and implications for precision oncology.Frontiers in oncology · 2026Review
- Out"FOX"ing cancer: the implications of FOXC2 as a putative predictive biomarker for cancer immunotherapy.Frontiers in medicine · 2026Article
- Insights into SUMOylation in gastric cancer: molecular mechanisms and emerging therapeutic opportunities.Journal of cancer research and clinical oncology · 2025Review
- Detection, molecular function and mechanisms of m5C in cancer.Clinical and translational medicine · 2025Review
- SENP3 mediates the activation of the Wnt/β-catenin signaling pathway to accelerate the growth and metastasis of oesophagal squamous cell carcinoma in mice.Functional & integrative genomics · 2024Article
- SENP3 Promotes Mantle Cell Lymphoma Development through Regulating Wnt10a Expression.Current medical science · 2024Article
- Myeloid SENP3 deficiency protects mice from diet and age-induced obesity via regulation of YAP1 SUMOylation.Cellular and molecular life sciences : CMLS · 2023Article
- The SUMOylation and ubiquitination crosstalk in cancer.Journal of cancer research and clinical oncology · 2023Review
- Role of non-canonical post-translational modifications in gastrointestinal tumors.Cancer cell international · 2023Review
- SUMOylation of TUFT1 is essential for gastric cancer progression through AKT/mTOR signaling pathway activation.Cancer science · 2023Article
- SENP2 Promotes VSMC Phenotypic Switching via Myocardin De-SUMOylation.International journal of molecular sciences · 2022Article
- Cancer-Associated Dysregulation of Sumo Regulators: Proteases and Ligases.International journal of molecular sciences · 2022Review
- 5-methylcytosine RNA methyltransferases and their potential roles in cancer.Journal of translational medicine · 2022Review
- Dissecting the effects of androgen deprivation therapy on cadherin switching in advanced prostate cancer: A molecular perspective.Oncology research · 2022Review
- SENP3 promotes tumor progression and is a novel prognostic biomarker in triple-negative breast cancer.Frontiers in oncology · 2022Article
- A Deep Neural Network for Gastric Cancer Prognosis Prediction Based on Biological Information Pathways.Journal of oncology · 2022Article
- MicroRNA‑199a‑5p regulates FOXC2 to control human vascular smooth muscle cell phenotypic switch.Molecular medicine reports · 2021Article
- SENP Proteases as Potential Targets for Cancer Therapy.Cancers · 2021Review
- SUMO: From Bench to Bedside.Physiological reviews · 2020Review
- A fine-tuning mechanism underlying self-control for autophagy: deSUMOylation of BECN1 by SENP3.Autophagy · 2020Article
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The impact of cellular oxidative stress in promoting the epithelial-mesenchymal transition (EMT) has been noticed. Our previous study shows that SENP3, a redox-sensitive SUMO2/3-specific protease, accumulates in a variety of cancers, but whether SENP3 and SUMOylation involve in the regulation of EMT is unclear. The present study uncovers a novel role of SENP3 in promoting the EMT process in gastric cancer via regulating an EMT-inducing transcription factor, forkhead box C2 (FOXC2). We demonstrate that the expression of mesenchymal marker genes and cell migration ability are enhanced in SENP3-overexpressing gastric cancer cells and attenuated in SENP3-knockdown cells. A nude mouse model and a set of patient's specimens suggest the correlation between SENP3 and gastric cancer metastasis. Biochemical assays identify FOXC2 as a substrate of SENP3. Meanwhile N-cadherin is verified as a target gene of FOXC2, which is transcriptionally activated by a SUMO-less FOXC2. Additionally, reactive oxygen species-induced de-SUMOylation of FOXC2 can be blocked by silencing endogenous SENP3. In conclusion, SENP3, which is increased in gastric cancer cells, potentiates the transcriptional activity of FOXC2 through de-SUMOylation, in favor of the induction of specific mesenchymal gene expression in gastric cancer metastasis.
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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.