ArticleOncotarget2016
SFMBT2 (Scm-like with four mbt domains 2) negatively regulates cell migration and invasion in prostate cancer cells.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 27 citations in OpenAlex.
- SFMBT2 hypermethylation promotes colorectal cancer progression and is a potential noninvasive biomarker for advanced CRC.iScience · 2026Article
- CRISPRi Screen Identifies a Novel Growth Suppressor lncRNA,bioRxiv : the preprint server for biology · 2025Article
- Review
- Acetylation- and ubiquitination-regulated SFMBT2 acts as a tumor suppressor in clear cell renal cell carcinoma.Biology direct · 2024Article
- A CIC-related-epigenetic factors-based model associated with prediction, the tumor microenvironment and drug sensitivity in osteosarcoma.Scientific reports · 2024Article
- Role of the TRP Channels in Pancreatic Ductal Adenocarcinoma Development and Progression.Cells · 2021Review
- circ‑0000212 promotes cell proliferation of colorectal cancer by sponging miR‑491 and modulating FOXP4 expression.Molecular medicine reports · 2021Article
- Epigenetic Deregulation of the Histone MethyltransferaseFrontiers in cell and developmental biology · 2021Article
- Article
- The protein secretion modulator TMED9 drives CNIH4/TGFα/GLI signaling opposing TMED3-WNT-TCF to promote colon cancer metastases.Oncogene · 2019Article
- The Two Sides of YY1 in Cancer: A Friend and a Foe.Frontiers in oncology · 2019Review
- TRPM2 promotes the proliferation and invasion of pancreatic ductal adenocarcinoma.Molecular medicine reports · 2018Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metastatic prostate cancer is the leading cause of morbidity and mortality in men. In this study, we found that expression level of SFMBT2 is altered during prostate cancer progression and has been associated with the migration and invasion of prostate cancer cells. The expression level of SFMBT2 is high in poorly metastatic prostate cancer cells compared to highly metastatic prostate cancer cells. We also found that SFMBT2 knockdown elevates MMP-2, MMP-3, MMP-9, and MMP-26 expression, leading to increased cell migration and invasion in LNCaP and VCaP cells. SFMBT2 interacts with YY1, RNF2, N-CoR and HDAC1/3, as well as repressive histone marks such as H3K9me2, H4K20me2, and H2AK119Ub which are associated with transcriptional repression. In addition, SFMBT2 knockdown decreased KAI1 gene expression through up-regulation of N-CoR gene expression. Expression of SFMBT2 in prostate cancer was strongly associated with clinicopathological features. Patients having higher Gleason score (≥ 8) had substantially lower SFMBT2 expression than patients with lower Gleason score. Moreover, tail vein or intraprostatic injection of SFMBT2 knockdown LNCaP cells induced metastasis. Taken together, our findings suggest that regulation of SFMBT2 may provide a new therapeutic strategy to control prostate cancer metastasis as well as being a potential biomarker of metastatic prostate cancer.
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