ArticleArchives of medical science : AMS2026
CXCR4/CXCR7 gene-silencing suppresses ovarian cancer cell proliferation and tumour growth through modulation of the CXCL12-CXCR4/CXCR7 chemokine axis and activation of MAPK signalling pathway.
Article in Archives of medical science : AMS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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6 authors.
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Abstract
Introduction: Ovarian cancer is the most common malignant cancer among females. This study aimed to investigate role of the CXCL12-CXCR4/CXCR7 chemokine axis in ovarian cancer. Material and methods: SKOV3 cells were transfected with siCXCR4/siCX-CR7 plasmids and divided into SKOV3, LV3, LV3-siCXCR4, and LV3-siCXCR7 groups. Cell viability and apoptosis were examined using MTT and flow cytometry. ELISA was conducted to evaluate vascular-endothelial growth factor-A (VEGF-A), interleukin-6 (IL-6), and interleukin-8 (IL-8) levels. SKOV3 cells were transplanted into mice to establish a Xenograft model. The tumour volume of the Xenograft model was recorded. CD31, matrix-metalloprotein-9 (MMP-9), vimentin, and E-cadherin expressions in SKOV3 cells and tumour tissues were evaluated with quantitative real-time PCR (qRT-PCR) and western blot. Immunohistochemistry assay was used to detect VEGF-A, CD31, MMP-9, vimentin, and E-cadherin expression. Results: SKOV3 cells strongly expressed CXCR4 and CXCR7. CXCL12 significantly enhanced cell viability, and CXCR4/CXCR7 inhibitor remarkably reduced cell viability of SKOV3 ( Conclusions: CXCR4/CXCR7 gene-silencing could suppress ovarian cancer cell proliferation and tumour growth through modulation of the CXCL12-CXCR4/CXCR7 chemokine axis and mitogen-activated protein kinase (MAPK) signalling pathway.
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