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Publication Date

Fall 12-10-2025

Keywords

Ewing Sarcoma, Pediatric Cancer, CXCR4, Chemokine Receptor, Extracellular Matrix, CRISPR, Apoptosis, Proliferation, Migration, qRTPCR, Incucyte, Tissue Culture

Description

C-X-C chemokine receptor type 4 (CXCR4) is a seven-transmembrane G-protein–coupled receptor (GPCR). When activated by its ligand SDF-1 (CXCL12), CXCR4 triggers signaling pathways that promote cell survival, proliferation, angiogenesis, and chemotaxis. Many cancers exploit the CXCR4/SDF-1 axis to support tumor growth and metastasis. Ewing sarcoma (ES8) is an aggressive pediatric bone and soft-tissue cancer, and elevated CXCR4 signaling has been linked to increased migration and metastatic behavior. ES8 cells, a well-established ES8 cell line, provided a model to study how CXCR4contributes to tumor progression. CRISPR-Cas9 genome editing was used to knock down CXCR4 in ES8 cells, delivered through lipid-based transfection. Lipofection allows Cas9 and guide RNA to enter the cell and introduce targeted gene disruption. This project evaluated how CXCR4 loss affects tumorigenic properties, including proliferation, colony formation, migration, and survival. We hypothesized that reducing CXCR4 expression would decrease these behaviors, given its established role in promoting aggressive and metastatic phenotypes in Ewing sarcoma.

Collection

Mechanisms of Disease Lab Reports

Format

pdf

Size or Duration

1

City

San Antonio

Creative Commons License

Creative Commons Attribution-Share Alike 4.0 International License
This work is licensed under a Creative Commons Attribution-Share Alike 4.0 International License.

How CXCR4 Knockdown Affects Tumorigenic Properties in ES8 Cells

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