Evidence map›Paper›PMID 32885593›Full record

ReviewJournal of cellular and molecular medicine2020

SATB2 is a novel biomarker and therapeutic target for cancer.

Sanjit K Roy, Anju Shrivastava, Sudesh Srivastav, Sharmila Shankar, Rakesh K Srivastava

Open access · goldAbstract readReview
In one paragraph

Review in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 12% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.

  1. Pooled it
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  5. Review
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  7. Cancer Stem Cells Shift Metabolite Acetyl-Coenzyme A to Abrogate the Differentiation of CD103Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  12. Profiling Genome-Wide Methylation Patterns in Cattle Infected withInternational journal of molecular sciences · 2024
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 1 country.

Sanjit K RoyStanley S. Scott Cancer Center, Louisiana State University Health Sciences Center, New Orleans, LA, USA.
Anju ShrivastavaSt. Joseph's Hospital and Medical Center, Phoenix, AZ, USA.
Sudesh SrivastavDepartment of Biostatistics and Data Science, School of Public Health and Tropical Medicine, Tulane University School of Medicine, New Orleans, LA, USA.
Sharmila ShankarStanley S. Scott Cancer Center, Louisiana State University Health Sciences Center, New Orleans, LA, USA.
Rakesh K SrivastavaStanley S. Scott Cancer Center, Louisiana State University Health Sciences Center, New Orleans, LA, USA.ORCID 0000-0003-3112-4252
Louisiana State University Health Sciences Center New Orleans · USTulane University · USSt. Joseph's Hospital and Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Several studies have confirmed the involvement of cancer stem cells (CSC) in tumour progression, metastasis, drug resistance and cancer relapse. SATB2 (special AT-rich binding protein-2) acts as a transcriptional co-factor and modulates chromatin architecture to regulate gene expression. The purpose of this review was to discuss the pathophysiological roles of SATB2 and assess whether it could be used as a therapeutic target for cancer. SATB2 modulated the expression of those genes which regulated pluripotency and self-renewal. Overexpression of SATB2 gene in normal epithelial cells was shown to induce transformation, as a result transformed cells gained CSC's characteristics by expressing stem cell markers and pluripotency maintaining factors, suggesting its role as an oncogene. In addition, SATB2 induced epithelial-mesenchymal transition (EMT) and metastasis. Interestingly, the expression of SATB2 was positively correlated with the activation of β-catenin/TCF-LEF pathway. Furthermore, SATB2 silencing inhibited EMT and their positive regulators, and tumour growth, and suppressed the expression of stem cell markers, pluripotency maintaining factors, cell cycle and cell survival genes, and TCF/LEF targets. Based on the cancer genome atlas (TCGA) expression data and published papers, SATB2 alone or in combination with other proteins could be used a diagnostic biomarker for cancer. Although there is no pharmacological inhibitor of SATB2, studies using genetic approaches suggest that SATB2 could be a potential target for cancer treatment and prevention.

Indexed as

Molecular Targeted TherapyAnimalsBiomarkers, TumorEpithelial-Mesenchymal TransitionHumansNeoplasmsNeoplastic Stem CellsTranscription FactorsBiomarkers, TumorTranscription Factorscancer stem cellsCD133CD24CD44c-MycLGR5NanogOct4pluripotencySATB2self-renewalSox2TCF/LEFβ-catenin

Identifiers

PMID32885593
PMCPMC7576221
OpenAlexW3083725095

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.