ArticleDiscover oncology2025
CXCR7 promoted proliferation, migration and invasion in HCC Cells by inactivating Hippo-YAP signaling.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed.
- High COMP expression promotes tumor cell proliferation and migration of rectal cancer, contributing to unfavorable prognosis and suppressive immune microenvironment.Discover oncology · 2026Article
- Epidemiology, molecular typing, microbiome-immune interactions and treatment strategies of endometrial cancer: a review.Frontiers in immunology · 2025Review
- CXCR7-TAGLN2 protein complex regulates invasion and metastasis in papillary thyroid carcinoma: a potential therapeutic target.Frontiers in immunology · 2025Article
- Chemokines in the resolution of inflammation: key players and targets for therapeutic modulation.Frontiers in immunology · 2025Review
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Authors and funding
5 authors.
Funding
Abstract
backgroundCXCR7 (ACKR3) has been well-supported as a promoter of growth and metastasis in hepatocellular carcinoma (HCC). Both CXCR7 and Hippo signaling play roles in organ development. We aimed to verify the involvement of Hippo-YAP signaling in CXCR7-regulated HCC proliferation, migration, and invasion.
methodsHCCLM3 cells were transfected with si-CXCR7, pcDNA-CXCR7, or related control RNA/empty vector. Cell proliferation was assessed using the Cell Counting Kit-8 (CCK-8), and mRNA and protein levels were measured via quantitative real-time PCR (qPCR) and Western blotting. Colony formation assays were conducted to evaluate proliferation capacity, and Transwell assays were used to assess invasion and migration. Transcriptome data from the TCGA-LIHC dataset were analyzed to investigate the potential effects of CXCR7 in HCC.
resultssi-CXCR7 inhibited cell proliferation in HCCLM3 cells, while pcDNA-CXCR7 promoted it. Migration and invasion were suppressed by si-CXCR7 but enhanced by pcDNA-CXCR7. Patients with higher CXCR7 expression in the TCGA-LIHC dataset had lower overall survival rates and increased gene transcription. The CXCR7-high expressing samples were characterized by the activation of several pathways, including PI3K-AKT signaling, calcium signaling, and the Hippo signaling pathway. si-CXCR7 reduced the relative protein levels of Gαq/11 and GαS while increasing phosphorylated LATS and phosphorylated YAP. Opposite trends in these proteins were observed with pcDNA-CXCR7. Finally, the inhibitory effects of si-CXCR7 on cell proliferation, migration, and invasion were reversed by the YAP inhibitor verteporfin.
conclusionWe suggest that CXCR7 promotes the growth and metastasis of HCC cells, at least in part, by inactivating the Hippo-YAP signaling pathway.
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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 Socratic graph.