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BIOMARKER:

CCL5 overexpression

i
Other names: CCL5, D17S136E, MGC17164, RANTES, SCYA5, SISd, TCP228, Chemokine (C-C motif) ligand 5
Entrez ID:
Related biomarkers:
1year
Fentanyl Promoted the Growth of Placenta Trophoblast Cells through Regulating the METTL14 Mediated CCL5 Levels. (PubMed, Biol Pharm Bull)
Additionally, METTL14 silenced prominently decreased the m6A and mRNA levels, along with the mRNA stability of CCL5. In conclusion, fentanyl promoted the growth and inhibited the apoptosis of the HG stimulated HTR8/SVneo cells through regulating the METTL14 mediated CCL5 levels.
Journal
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TNFA (Tumor Necrosis Factor-Alpha) • CCL5 (Chemokine (C-C motif) ligand 5) • IL10 (Interleukin 10) • IL1B (Interleukin 1, beta) • METTL14 (Methyltransferase 14)
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CCL5 overexpression • IL10 elevation
almost3years
Association of CC chemokines with breast cancer disparity (AACR 2022)
Furthermore, higher CCR9 expressing cells showed poor response to Carboplatin upon CCR9 activation. In conclusion, our data suggest the association of distinct CC-chemokines in BrCa progression, OS, and disparate disease outcome in AA compared to EA patients implying CCR9 signaling to be a potential target for improving chemotherapeutic response.
BRCA Biomarker
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HER-2 (Human epidermal growth factor receptor 2) • CCL20 (C-C Motif Chemokine Ligand 20) • CCL5 (Chemokine (C-C motif) ligand 5) • CCL11 (C-C Motif Chemokine Ligand 11) • CCL2 (Chemokine (C-C motif) ligand 2) • CCL22 (C-C Motif Chemokine Ligand 22) • CCL7 (Chemokine (C-C motif) ligand 7)
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HER-2 expression • CCL5 overexpression • CCL7 expression • CCL7 overexpression
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carboplatin
almost3years
CCL5 secreted by luminal B breast cancer cells induces polarization of M2 macrophages through activation of MEK/STAT3 signaling pathway via CCR5. (PubMed, Gene)
Furthermore, we studied its interaction with CCR5 and MEK/STAT3 signaling members. These targets could be used as key regulatory members in human breast cancer therapy.
Journal
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HER-2 (Human epidermal growth factor receptor 2) • CCL5 (Chemokine (C-C motif) ligand 5) • STAT2 (Signal transducer and activator of transcription 2)
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HER-2 expression • CCL5 overexpression
over3years
Anti-tumor immunity in mismatch repair-deficient colorectal cancers requires type I IFN-driven CCL5 and CXCL10. (PubMed, J Exp Med)
CCL5 and CXCL10 could be up-regulated by common chemotherapies in all CRCs, indicating that facilitating CD8+ T cell recruitment underlies their efficacy. Induction of CCL5 and CXCL10 thus represents a tractable therapeutic strategy to induce TIL recruitment into CRCs, where local priming can be maximized even in neoantigen-poor CRCs.
Journal • Mismatch repair
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CD8 (cluster of differentiation 8) • CXCL10 (Chemokine (C-X-C motif) ligand 10) • STING (stimulator of interferon response cGAMP interactor 1) • CCL5 (Chemokine (C-C motif) ligand 5)
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MSI-H/dMMR • CCL5 overexpression
over3years
Dissecting spatial heterogeneity and the immune-evasion mechanism of CTCs by single-cell RNA-seq in hepatocellular carcinoma. (PubMed, Nat Commun)
Mechanistically, overexpression of CCL5 in CTCs is transcriptionally regulated by p38-MAX signaling, which recruites regulatory T cells (Tregs) to facilitate immune escape and metastatic seeding of CTCs. Collectively, our results reveal a previously unappreciated spatial heterogeneity and an immune-escape mechanism of CTC, which may aid in designing new anti-metastasis therapeutic strategies in HCC.
Journal
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CCL5 (Chemokine (C-C motif) ligand 5)
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CCL5 overexpression