ArticlePloS one2013
RETRACTED: Upregulation of SATB1 is associated with prostate cancer aggressiveness and disease progression.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 23 papers, 1 of them a synthesis that pooled it.
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
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- SATB1 overexpression correlates with gastrointestinal neoplasms invasion and metastasis: a meta-analysis for Chinese population.Oncotarget · 2017Pooled it
- Urinary miR-191-5p levels are significantly reduced after radical prostatectomy in patients with prostate cancer.Cancer cell international · 2026Article
- Retraction: Upregulation of SATB1 Is Associated with Prostate Cancer Aggressiveness and Disease Progression.PloS one · 2026Article
- SATB1 in cancer progression and metastasis: mechanisms and therapeutic potential.Frontiers in oncology · 2025Review
- Adaptive and non-adaptive gene expression responses in prostate cancer during androgen deprivation.PloS one · 2023Article
- SATB1, genomic instability and Gleason grading constitute a novel risk score for prostate cancer.Scientific reports · 2021Article
- SATB1 protein is associated with the epithelial‑mesenchymal transition process in non‑small cell lung cancers.Oncology reports · 2021Article
- The Role of SATB1 in Tumour Progression and Metastasis.International journal of molecular sciences · 2019Review
- PAK5 promotes the migration and invasion of cervical cancer cells by phosphorylating SATB1.Cell death and differentiation · 2019Article
- Divergent SATB1 expression across human life span and tissue compartments.Immunology and cell biology · 2019Article
- Assessment of the Utility of Gene Positioning Biomarkers in the Stratification of Prostate Cancers.Frontiers in genetics · 2019Article
- Inhibition of prostate cancer cell growthOncology letters · 2017Article
- SATB1 plays an oncogenic role in esophageal cancer by up-regulation of FN1 and PDGFRB.Oncotarget · 2017Article
- A four gene signature predictive of recurrent prostate cancer.Oncotarget · 2017Article
- Analysis of cellular and molecular antitumor effects upon inhibition of SATB1 in glioblastoma cells.BMC cancer · 2017Article
- Special AT-rich DNA-binding protein-1 expression is associated with liver cancer metastasis.Oncology letters · 2016Article
- Effect of silencing SATB1 on proliferation, invasion and apoptosis of A549 human lung adenocarcinoma cells.Oncology letters · 2016Article
- Baicalein suppresses metastasis of breast cancer cells by inhibiting EMT via downregulation of SATB1 and Wnt/β-catenin pathway.Drug design, development and therapy · 2016Article
- SATB1 and 2 in colorectal cancer.Carcinogenesis · 2015Review
- SATB1 overexpression regulates the development and progression in bladder cancer through EMT.PloS one · 2015Article
Corrections and comments
- Retraction · 2026-03-12Concerns/Issues about Animal Welfare · Concerns/Issues about Data · Concerns/Issues about Image · Concerns/Issues about Methods · Concerns/Issues about Results and/or Conclusions · Error in Analyses · Lack of IRB/IACUC Approval and/or Compliance · Objections by Author(s) · · See also: https://pubpeer.com/publications/A45B9844F593C50F549BBDDB6DC5AF
- Retracted
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Disease aggressiveness remains a critical factor to the progression of prostate cancer. Transformation of epithelial cells to mesenchymal lineage, associated with the loss of E-cadherin, offers significant invasive potential and migration capability. Recently, Special AT-rich binding protein (SATB1) has been linked to tumor progression. SATB1 is a cell-type restricted nuclear protein, which functions as a tissue-specific organizer of DNA sequences during cellular differentiation. Our results demonstrate that SATB1 plays significant role in prostate tumor invasion and migration and its nuclear localization correlates with disease aggressiveness. Clinical specimen analysis showed that SATB1 was predominantly expressed in the nucleus of high-grade tumors compared to low-grade tumor and benign tissue. A progressive increase in the nuclear levels of SATB1 was observed in cancer tissues compared to benign specimens. Similarly, SATB1 protein levels were higher in a number of prostate cancer cells viz. HPV-CA-10, DU145, DUPro, PC-3, PC-3M, LNCaP and C4-2B, compared to non-tumorigenic PZ-HPV-7 cells. Nuclear expression of SATB1 was higher in biologically aggressive subclones of prostate cancer cells with their respective parental cell lines. Furthermore, ectopic SATB1 transfection conferred increased cell motility and invasiveness in immortalized human prostate epithelial PZ-HPV-7 cells which correlated with the loss of E-cadherin expression. Consequently, knockdown of SATB1 in highly aggressive human prostate cancer PC-3M cells inhibited invasiveness and tumor growth in vivo along with increase in E-cadherin protein expression. Our findings demonstrate that SATB1 has ability to promote prostate cancer aggressiveness through epithelial-mesenchymal transition.
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.