ArticleOncoTargets and therapy2019
Impact of CXCR4 and CXCR7 knockout by CRISPR/Cas9 on the function of triple-negative breast cancer cells.
Article in OncoTargets and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.
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Who cites it
33 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.
- The mechanism of breast cancer stem cells and tumor microenvironment promoting radioresistance in breast cancer and its intervention strategies.Frontiers in immunology · 2026Pooled it
- CXCL12/ZNF503/GATA3/MMP1 axis promotes tumor progression and metastasis of triple-negative breast cancer.Breast cancer research : BCR · 2026Article
- DEC1 promotes breast cancer bone metastasis through transcriptional activation of CXCR4.Journal of biomedical research · 2025Article
- Novel strategies to overcome tumor immunotherapy resistance using CAR NK cells.Frontiers in immunology · 2025Review
- Connexin 43 hemichannels and related diseases.Antibody therapeutics · 2024Review
- From Biosensors to Robotics: Pioneering Advances in Breast Cancer Management.Sensors (Basel, Switzerland) · 2024Review
- CRISPR-Based Gene Editing: a Modern Approach for Study and Treatment of Cancer.Applied biochemistry and biotechnology · 2024Review
- CRISPR/Cas9 systems: Delivery technologies and biomedical applications.Asian journal of pharmaceutical sciences · 2023Review
- The various role of microRNAs in breast cancer angiogenesis, with a special focus on novel miRNA-based delivery strategies.Cancer cell international · 2023Review
- CRISPR/Cas9 as a therapeutic tool for triple negative breast cancer: from bench to clinics.Frontiers in molecular biosciences · 2023Review
- Current updates of CRISPR/Cas9-mediated genome editing and targeting within tumor cells: an innovative strategy of cancer management.Cancer communications (London, England) · 2022Review
- Nanomaterial-assisted CRISPR gene-engineering - A hallmark for triple-negative breast cancer therapeutics advancement.Materials today. Bio · 2022Review
- CRISPR/Cas9 system in breast cancer therapy: advancement, limitations and future scope.Cancer cell international · 2022Review
- Functional Tumor Targeting Nano-Systems for Reprogramming Circulating Tumor Cells with In Situ Evaluation on Therapeutic Efficiency at the Single-Cell Level.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Strategies to overcome the main challenges of the use of CRISPR/Cas9 as a replacement for cancer therapy.Molecular cancer · 2022Review
- Associations of CXCL12 polymorphisms with clinicopathological features in breast cancer: a case-control study.Molecular biology reports · 2022Article
- Article
- Peptide Nanoparticle-Mediated Combinatorial Delivery of Cancer-Related siRNAs for Synergistic Anti-Proliferative Activity in Triple Negative Breast Cancer Cells.Pharmaceuticals (Basel, Switzerland) · 2021Article
- ATP Inhibits Breast Cancer Migration and Bone Metastasis through Down-Regulation of CXCR4 and Purinergic Receptor P2Y11.Cancers · 2021Article
- Drivers and suppressors of triple-negative breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBreast cancer is one of the most common malignancies threatening women's health. Triple-negative breast cancer (TNBC) is a special type of breast cancer with high invasion and metastasis. CXCL12 and its receptors CXCR4 and CXCR7 play a crucial role in the progress of breast cancer. The aim of this study was to investigate the effect of CXCR4 and CXCR7 on the function of TNBC. MATERIALS AND
methodsWe used the CRISPR/Cas9 technique to carry out a single knockout of the CXCR4 or CXCR7 gene and co-knockout of CXCR4 and CXCR7 genes in the TNBC cell line (MDA-MB-231). The single knockout and co-knockout cells were screened and verified by PCR sequencing and Western blot assay, the effect of single knockout and co-knockout on the proliferation of TNBC cells was examined using the Cell Counting Kit-8 and colony formation assays, the migration and invasion of TNBC cells were examined by the transwell and wound-healing assays, the changes in the cell cycle distribution after knockout were detected by flow cytometry, and the difference in the migration and invasion of single knockout and co-knockout induced by CXCL12 was observed by adding CXCL12 in the experimental group.
resultsThe single knockout of the CXCR4 or CXCR7 gene significantly reduced the cell proliferation, growth, migration, and invasion and delayed the conversion of the G1/S cycle, while the co-knockout inhibited these biological abilities more significantly. In both the knockout and control groups, the migration and invasion of CXCL12-added cells were significantly stronger than those of the non-CXCL12-added cells, and CXCL12 induced lesser migration and invasion in the CXCR4 and CXCR7 co-knockout group than in the single knockout groups.
conclusionThe knockout of the CXCR4 and CXCR7 genes affects the binding capacity and functions of CXCL12, inhibits the malignant progression of TNBC cells significantly, and may become a potential target for the treatment of TNBC.
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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.