ArticleCancer science2010
Overexpression and involvement of special AT-rich sequence binding protein 1 in multidrug resistance in human breast carcinoma cells.
Article in Cancer science, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 51 citations in OpenAlex.
- SATB1 in cancer progression and metastasis: mechanisms and therapeutic potential.Frontiers in oncology · 2025Review
- Special AT-rich sequence binding protein 1 promotes multidrug resistance in gastric cancer by regulation of Ezrin to alter subcellular localization of ATP-binding cassette transporters.Cancer science · 2023Article
- Epigenetic Mechanisms beyond Tumour-Stroma Crosstalk.Cancers · 2021Review
- SATB1 Knockdown Inhibits Proliferation and Invasion and Decreases Chemoradiation Resistance in Nasopharyngeal Carcinoma Cells by Reversing EMT and Suppressing MMP-9.International journal of medical sciences · 2021Article
- An analysis of mutational signatures of synonymous mutations across 15 cancer types.BMC medical genetics · 2019Article
- HER2, NF-Disease markers · 2019Article
- Silencing SATB1 overcomes temozolomide resistance by downregulating MGMT expression and upregulating SLC22A18 expression in human glioblastoma cells.Cancer gene therapy · 2018Article
- iTextMine: integrated text-mining system for large-scale knowledge extraction from the literature.Database : the journal of biological databases and curation · 2018Article
- P53-miR-191-RNA (New York, N.Y.) · 2017Article
- Inhibition of apoptosis by oncogenic hepatitis B virus X protein: Implications for the treatment of hepatocellular carcinoma.World journal of hepatology · 2016Review
- SATB1 is a potential therapeutic target in intrahepatic cholangiocarcinoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2016Article
- SATB1 Promotes Pancreatic Cancer Growth and Invasion Depending on MYC Activation.Digestive diseases and sciences · 2015Article
- Divergent expression patterns of SATB1 mRNA and SATB1 protein in colorectal cancer and normal tissues.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- Expression of SATB1 and HER2 in breast cancer and the correlations with clinicopathologic characteristics.Diagnostic pathology · 2015Article
- SATB1 Mediates Long-Range Chromatin Interactions: A Dual Regulator of Anti-Apoptotic BCL2 and Pro-Apoptotic NOXA Genes.PloS one · 2015Article
- Overexpression of miR-21-5p as a predictive marker for complete tumor regression to neoadjuvant chemoradiotherapy in rectal cancer patients.BMC medical genomics · 2014Article
- Role of tissue-specific AT-rich DNA sequence-binding proteins in lymphocyte differentiation.International journal of hematology · 2014Review
- The haplotype of three polymorphisms in theOncology letters · 2014Article
- Inhibition of SATB1 by shRNA suppresses the proliferation of cutaneous malignant melanoma.Cancer biotherapy & radiopharmaceuticals · 2014Article
- Silencing SATB1 inhibits the malignant phenotype and increases sensitivity of human osteosarcoma U2OS cells to arsenic trioxide.International journal of medical sciences · 2014Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Special AT-rich sequence binding protein (SATB) 1 has been proposed to act as a determinant for the acquisition of metastatic activity by controlling expression of a specific set of genes that promote metastatic activity. Here we found that SATB1 expression is upregulated in multidrug-resistant breast cancer cells that exhibit higher invasive potential than the parental cells. Apart from accelerating metastasis and inducing epithelial-mesenchymal transition, SATB1 was demonstrated to confer resistance to both P-glycoprotein-related and P-glycoprotein-non-related drugs on MCF7 cells, which was accompanied by decreasing accumulation of adriamycin in SATB1-overexpressing transfectants. SATB1 depletion could partially reverse the multidrug resistance (MDR) phenotype of MCF7/ADR in vitro and in vivo. The SATB1-induced P-glycoprotein-mediated MDR could be reversed by treatment with anti-P-glycoprotein mAb. Moreover, SATB1 plays an important role in anti-apoptotic activity in MCF7/ADR cells in response to adriamycin treatment, which suggests another mechanism contributing to SATB1-related MDR of breast cancers. These data provide new insights into the mode by which breast tumors acquire the MDR phenotype and also imply a role for SATB1 in this process.
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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.