ArticleCell death & disease2019
CXCL5 induces tumor angiogenesis via enhancing the expression of FOXD1 mediated by the AKT/NF-κB pathway in colorectal cancer.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers, 1 of them a synthesis that pooled it.
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Who cites it
109 citing papers in PubMed, 1 synthesis or guideline pooled it, 159 citations in OpenAlex.
- CXCL5: A coachman to drive cancer progression.Frontiers in oncology · 2022Pooled it
- Celecoxib as an adjuvant to chemotherapy for patients with metastatic colorectal cancer: A randomized controlled clinical study.Saudi medical journal · 2022Trial
- Cellular senescence: six decades of discovery and reinvention.The EMBO journal · 2026Review
- Transcription Factor HOXC11 Drives Colorectal Cancer Progression and Metastasis via CAMK2A-Dependent CXCL5 Upregulation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- PSPH Promotes Hepatocellular Carcinoma Progression by Upregulating HIF-1α and Is Regulated by LncRNA GSEC/miR-101-3p.Current issues in molecular biology · 2026Article
- Epigenetic dynamics of cellular senescence: From mechanistic insights to precision senotherapy.Chinese medical journal · 2026Review
- The hypoxic ECM and neutrophils in MIBC immunotherapy resistance.Nature reviews. Urology · 2026Review
- CXCL5 suppresses osteoclastogenesis and protects against lipoteichoic acid-induced bone loss by modulating PLCγ2 and c-Fos signalling in gram-positive periprosthetic joint infection.Bone & joint research · 2026Article
- Decoding Colorectal Cancer: Key Genes and Pathways in the Chinese Population Revealed.Current medicinal chemistry · 2026Article
- Identification of a Novel PDRG1-EZH2-p21 Pathway Controlling Senescence and Tumor Progression in Hepatocellular Carcinoma.International journal of biological sciences · 2026Article
- Agonist signaling drives neutrophil subpopulations to promote/inhibit colorectal cancer liver metastasis.Nature communications · 2025Article
- CXCL5 neutralization mitigates cancer cachexia by disrupting CAF-cancer cell crosstalk.Journal of biomedical science · 2025Article
- FOXD1, a hypoxia-related gene, accelerates prostate cancer cell growth by increasing glycolysis under hypoxia conditions.BMC biotechnology · 2025Article
- Scavenging acrolein with 2-HDP preserves neurovascular integrity in a rat model of diabetic retinal disease.Diabetologia · 2025Article
- Article
- The states of senescent cells.Biochemical Society transactions · 2025Review
- Dual-faced CXCL5 holds the key to unlocking immunotherapy in obese pancreatic cancer.Journal for immunotherapy of cancer · 2025Article
- Cellular senescence and other age-related mechanisms in skeletal diseases.Bone research · 2025Review
- Article
- Tumor-derived CXCL5 promotes 5-fluorouracil resistance in colorectal cancer cells via p21 downregulation.Medical oncology (Northwood, London, England) · 2025Article
49 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanisms underlying the role of CXCL5 in tumor angiogenesis have not been fully defined. Here, we examined the effect of CXCL5 on tumor angiogenesis in colorectal cancer (CRC). Immunohistochemistry was used to monitor the expression of CXCL5 and CD31 in CRC patients' tissues. HUVEC cell lines stably transfected with shCXCR2 and shFOXD1 lentivirus plasmids were used in an in vitro study. Based on some molecular biological experiments in vitro and in vivo, we found that CXCL5 was upregulated in tumor tissues and that its level positively correlated with the expression of CD31. Next, we used recombinant human CXCL5 (rhCXCL5) to stimulate HUVECs and found that their tube formation ability, proliferation, and migration were enhanced by the activation of the AKT/NF-κB/FOXD1/VEGF-A pathway in a CXCR2-dependent manner. However, silencing of CXCR2 and FOXD1 or inhibition of the AKT and NF-κB pathways could attenuate the tube formation ability, proliferation, and migration of rhCXCL5-stimulated HUVECs in vitro. rhCXCL5 can promote angiogenesis in vivo in Matrigel plugs, and the overexpression of CXCL5 can also increase microvessel density in vivo in a subcutaneous xenotransplanted tumor model in nude mice. Taken together, our findings support CXCL5 as an angiogenic factor that can promote cell metastasis through tumor angiogenesis in CRC. Furthermore, we propose that FOXD1 is a novel regulator of VEGF-A. These observations open new avenues for therapeutic application of CXCL5 in tumor anti-angiogenesis.
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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.