ArticleBMC molecular biology2016
Knockdown of SALL4 inhibits the proliferation and reverses the resistance of MCF-7/ADR cells to doxorubicin hydrochloride.
Article in BMC molecular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 26 citations in OpenAlex.
- An InDel Genomic Variant within a Bifunctional Super-Enhancer for LINC00636 and CD47 Regulation in Breast Cancer.Research square · 2026Article
- An InDel Genomic Variant within a Bifunctional Super-Enhancer for LINC00636 and CD47 Regulation in Breast Cancer.bioRxiv : the preprint server for biology · 2025Article
- Alectinib and SALL4-Targeted Fatty Acid Oxidation: A Strategy to Combat Oxaliplatin Resistance in Gastric Cancer.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2025Article
- The new advance of SALL4 in cancer: Function, regulation, and implication.Journal of clinical laboratory analysis · 2023Review
- Role of SALL4 in HER2+ Breast Cancer Progression: Regulating PI3K/AKT Pathway.International journal of molecular sciences · 2022Article
- Review
- SALL4 Oncogenic Function in Cancers: Mechanisms and Therapeutic Relevance.International journal of molecular sciences · 2022Review
- Role ofMolecular biology research communications · 2021Article
- Quantitative site- and structure-specific N-glycoproteomics characterization of differential N-glycosylation in MCF-7/ADR cancer stem cells.Clinical proteomics · 2020Article
- Novel Quinoline-based Ir(III) Complexes Exhibit High Antitumor ActivityACS medicinal chemistry letters · 2019Article
- SALL4 induces radioresistance in nasopharyngeal carcinoma via the ATM/Chk2/p53 pathway.Cancer medicine · 2019Article
- miR-125b regulates the drug-resistance of breast cancer cells to doxorubicin by targeting HAX-1.Oncology letters · 2018Article
- Knockdown of SALL4 overcomes cisplatin-resistance through AKT/mTOR signaling in lung cancer cells.International journal of clinical and experimental pathology · 2018Article
- SALL4 promotes glycolysis and chromatin remodeling via modulating HP1α-Glut1 pathway.Oncogene · 2017Article
- SALL4 suppresses PTEN expression to promote glioma cell proliferation via PI3K/AKT signaling pathway.Journal of neuro-oncology · 2017Article
- Knockdown of SALL4 Inhibits Proliferation, Migration, and Invasion in Osteosarcoma Cells.Oncology research · 2017Article
- Article
- Article
- Multi-omics approach to infer cancer therapeutic targets on chromosome 20q across tumor types.Advances in modern oncology researchArticle
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBreast cancer is the most frequent malignancy in women and drug resistance is the major obstacle for its successful chemotherapy. In the present study, we analyzed the involvement of an oncofetal gene, sal-like 4 (SALL4), in the tumor proliferation and drug resistance of human breast cancer.
resultsOur study showed that SALL4 was up-regulated in the drug resistant breast cancer cell line, MCF-7/ADR, compared to the other five cell lines. We established the lentiviral system expressing short hairpin RNA to knockdown SALL4 in MCF-7/ADR cells. Down-regulation of SALL4 inhibited the proliferation of MCF-7/ADR cells and induced the G1 phase arrest in cell cycle, accompanied by an obvious reduction of the expression of cyclinD1 and CDK4. Besides, down-regulating SALL4 can re-sensitize MCF-7/ADR to doxorubicin hydrochloride (ADMh) and had potent synergy with ADMh in MCF-7/ADR cells. Depletion of SALL4 led to a decrease in IC50 for ADMh and an inhibitory effect on the ability to form colonies in MCF-7/ADR cells. With SALL4 knockdown, ADMh accumulation rate of MCF-7/ADR cells was increased, while the expression of BCRP and c-myc was significantly decreased. Furthermore, silencing SALL4 also suppressed the growth of the xenograft tumors and reversed their resistance to ADMh in vivo.
conclusionSALL4 knockdown inhibits the growth of the drug resistant breast cancer due to cell cycle arrest and reverses tumor chemo-resistance through down-regulating the membrane transporter, BCPR. Thus, SALL4 has potential as a novel target for the treatment of breast cancer.
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