ArticleInternational journal of molecular sciences2013
Vascular endothelial growth factor induces CXCL1 chemokine release via JNK and PI-3K-dependent pathways in human lung carcinoma epithelial cells.
Article in International journal of molecular sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 35 citations in OpenAlex.
- The Clinical Significance and Involvement in Molecular Cancer Processes of Chemokine CXCL1 in Selected Tumors.International journal of molecular sciences · 2024Review
- Regulation of cancer stem cells by CXCL1, a chemokine whose secretion is controlled by MCM2.BMC cancer · 2024Article
- CXCL1 promotes cell migration in hepatocellular carcinoma by regulating the miR-30b-5p/ICAM-1 axis.Journal of Cancer · 2024Article
- TGFβ1 induces CXCL1 to promote stemness features in lung cancer.Experimental biology and medicine (Maywood, N.J.) · 2023Article
- Article
- CCL25 Signaling in the Tumor Microenvironment.Advances in experimental medicine and biology · 2021Article
- Cancer-Associated Muscle Wasting-Candidate Mechanisms and Molecular Pathways.International journal of molecular sciences · 2020Review
- CXCL1 as an Unfavorable Prognosis Factor Negatively Regulated by DACH1 in Non-small Cell Lung Cancer.Frontiers in oncology · 2019Article
- Chemokine (C-X-C motif) ligand 1 and CXCL2 produced by tumor promote the generation of monocytic myeloid-derived suppressor cells.Cancer science · 2018Article
- Tumor-derived cytokines impair myogenesis and alter the skeletal muscle immune microenvironment.Cytokine · 2018Article
- CXCL1 Is Critical for Premetastatic Niche Formation and Metastasis in Colorectal Cancer.Cancer research · 2017Article
- Sunitinib Treatment Enhances Metastasis of Innately Drug-Resistant Breast Tumors.Cancer research · 2017Article
- Protein phosphatase 2A activation attenuates inflammation in murine models of acute lung injury.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Chemokine CXCL1 may serve as a potential molecular target for hepatocellular carcinoma.Cancer medicine · 2016Article
- Genistein inhibits A549 human lung cancer cell proliferation via miR-27a and MET signaling.Oncology letters · 2016Article
- Volatile anaesthetics enhance the metastasis related cellular signalling including CXCR2 of ovarian cancer cells.Oncotarget · 2016Article
- Chemokines and their receptors in lung cancer progression and metastasis.Journal of Zhejiang University. Science. B · 2016Review
- γ-Secretase Activity Is Required for Regulated Intramembrane Proteolysis of Tumor Necrosis Factor (TNF) Receptor 1 and TNF-mediated Pro-apoptotic Signaling.The Journal of biological chemistry · 2016Article
- Article
- Inflammatory microenvironment and expression of chemokines in hepatocellular carcinoma.World journal of gastroenterology · 2015Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung cancer cells express different chemokines and chemokine receptors that modulate leukocyte infiltration within tumor microenvironment. In this study we screened several mediators/growth factors on CXCL1 release in human carcinoma epithelial cells. Of the tested mediators, VEGF was found to have a robust increase in causing CXCL1 release. VEGF stimulated CXCL1 release and mRNA expression in a time- and concentration-dependent manner. The release was inhibited by the VEGF receptor antagonists and the JNK, PI-3K, tyrosine kinase, and transcription inhibitors. In parallel, VEGF induced JNK, PI3K and Akt activation. Strikingly, among these inhibitors only the JNK inhibitor could reduce VEGF-induced CXCL1 mRNA expression, suggesting that JNK participated in VEGF-induced CXCL1 synthesis, whereas PI-3K was responsible for cellular CXCL1 secretory process. In addition, the steroid dexamethasone and TGF-β suppressed CXCL1 release through a transcriptional regulation. We also showed that cells stimulated with VEGF significantly attracted monocyte migration, which could be abolished by CXCL1 B/N Ab, CXC receptor 2 antagonist, TGF-β, and dexamethasone. In summary, we provide here evidence showing JNK activation for VEGF-induced CXCL1 DNA transcription and PI-3K pathway for extracellular CXCL1 release in human carcinoma epithelial cells. The released CXCL1 was functionally linked to recruiting monocytes into lung cancer cell microenvironment.
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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.