ArticleAmerican journal of cancer research2015
Chemokine CCL17 induced by hypoxia promotes the proliferation of cervical cancer cell.
Article in American journal of cancer research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 30 citations in OpenAlex.
- Suppressive effects on metastasis and tumor growth by the knockout of chemokine receptors in a canine cutaneous lymphoma model.The Journal of veterinary medical science · 2026Article
- Construction and validation of a chemokine-related gene signature associated with prognosis, clinical significance, and immune microenvironment characteristics in cervical cancer.Discover oncology · 2025Article
- The expression of CCL17 and potential prognostic value on tumor immunity in thyroid carcinoma based on bioinformatics analysis.Scientific reports · 2024Article
- CC Chemokine Family Members' Modulation as a Novel Approach for Treating Central Nervous System and Peripheral Nervous System Injury-A Review of Clinical and Experimental Findings.International journal of molecular sciences · 2024Review
- Activation of the CCL22/CCR4 causing EMT process remodeling under EZH2-mediated epigenetic regulation in cervical carcinoma.Journal of Cancer · 2024Article
- CC Chemokine Receptor 4 (CCR4) as a Possible New Target for Therapy.International journal of molecular sciences · 2022Review
- Circulating cytokines present in multiple myeloma patients inhibit the osteoblastic differentiation of adipose stem cells.Leukemia · 2022Article
- Comprehensive Analysis of Ferroptosis- and Immune-Related Signatures to Improve the Prognosis and Diagnosis of Kidney Renal Clear Cell Carcinoma.Frontiers in immunology · 2022Article
- A Novel Pyroptosis-Related Prognostic Signature for Cervical Squamous Cell Carcinoma.International journal of general medicine · 2022Article
- The Role of Chemokines in Cervical Cancers.Medicina (Kaunas, Lithuania) · 2021Review
- Tumour angiogenesis normalized by myo-inositol trispyrophosphate alleviates hypoxia in the microenvironment and promotes antitumor immune response.Journal of cellular and molecular medicine · 2021Article
- Identification of a Six-Gene Signature for Predicting the Overall Survival of Cervical Cancer Patients.OncoTargets and therapy · 2021Article
- CC Chemokines in a Tumor: A Review of Pro-Cancer and Anti-Cancer Properties of the Ligands of Receptors CCR1, CCR2, CCR3, and CCR4.International journal of molecular sciences · 2020Review
- Recombinant CCL17 Enhances Hematoma Resolution and Activation of CCR4/ERK/Nrf2/CD163 Signaling Pathway After Intracerebral Hemorrhage in Mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2020Article
- Manipulation of JAK/STAT Signalling by High-Risk HPVs: Potential Therapeutic Targets for HPV-Associated Malignancies.Viruses · 2020Review
- Hypoxia Alters the Expression of CC Chemokines and CC Chemokine Receptors in a Tumor-A Literature Review.International journal of molecular sciences · 2020Review
- Loss of GRHL3 leads to TARC/CCL17-mediated keratinocyte proliferation in the epidermis.Cell death & disease · 2018Article
- CCL17/TARC and CCR4 expression in Merkel cell carcinoma.Oncotarget · 2018Article
- CCR4 is a determinant of melanoma brain metastasis.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cervical cancer is often associated with hypoxia and many kinds of chemokines. But the relationship and role of hypoxia and Chemokine (C-C motif) ligand 17 (CCL17) in cervical cancer are still unknown. Here, we found that CCL17 was high expressed in cervical cancer. HeLa and SiHa cells could secrete CCL17 in a time-dependent manner. Hypoxia increased expression of CCL17 receptor (CCR4) on HeLa and SiHa cells. Treatment with recombination human CCL17 (rhCCL17) led to an elevation of cell proliferation in HeLa and SiHa cells in a dose-dependent manner. In contrast, blocking CCL17 with anti-human CCL17 neutralizing antibody (α-CCL17) played an oppose effect. However, rhCCL17 had no effect on apoptosis in cervical cancer cells. Further analysis showed that hypoxia promoted the proliferation of HeLa and SiHa cells, and these effects could be reversed by α-CCL17. Stimulation with the inhibitor for c-Jun N-terminal kinase (JNK) or signal transducers and activator of transcription 5 (STAT5) signal pathway not only directly decreased the proliferation of HeLa and SiHa cells, but also abrogated the stimulatory effect of rhCCL17 on the proliferation of HeLa and SiHa cells. These results suggest that a high level of CCL17 in cervical cancer lesions is an important regulator in the proliferation of cervical cancer cells through JNK and STAT5 signaling pathways. In this process, hypoxia magnifies this effect by up-regulating CCR4 expression and strengthening the interaction of CCL17/CCR4.
Indexed as
Identifiers
26693060PMC4656731W2418361431What OpenQuestion holds
Registered trials
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