SDF‑1/CXCR4 induces cell invasion through CD147 in squamous cell carcinoma of the hypopharynx

Toyoma, Satoshi; Suzuki, Shinsuke; Kawasaki, Yohei; Yamada, Tetsuji

doi:10.3892/ol.2020.11744

Cited by 6 publications

(3 citation statements)

References 49 publications

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“…Inhibition of the chemotaxis, proliferation, and fibrous transformation of circulating fibrocytes can help reduce airway basement membrane thickening [ 7 ]. TGF-β1 and CXCR4/CXCL12 signaling pathway have been shown to affect proliferation, differentiation, and chemotaxis of circulating fibrocytes [ 6 ], while CD147 has been reported to affect TGF-β1-mediated cell differentiation and CXCR4/CXCL12 signal transduction pathway [ 11 , 12 ]. However, whether CD147 affects the recruitment and activation of circulating fibrocytes are largely unclear.…”

Section: Discussionmentioning

confidence: 99%

“…CD147, alternatively referred to as EMMPRIN or Basigin [ 8 ], is a transmembrane glycoprotein of the immunoglobulin superfamily, and its upregulation is related to the pathogenesis of asthma and lung inflammatory disease [ 9 ]. CD147 has been reported to be involved in the regulation of fibroblast activation and ECM homeostasis [ 10 ], as well as cell differentiation induced by TGF-β1 [ 11 ], and activation of the CXCR4/CXCL12 signaling pathway [ 12 ]. Treatment with anti-CD147 monoclonal antibody (mAb) can reduce lung inflammation and airway mucus secretion in asthmatic mice [ 13 ].…”

Section: Introductionmentioning

confidence: 99%

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CD147 induces asthmatic airway remodeling and activation of circulating fibrocytes in a mouse model of asthma

Li,

Cheng,

Guo

et al. 2024

Respir Res

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Background Airway remodeling is a poorly reversible feature of asthma which lacks effective therapeutic interventions. CD147 can regulate extracellular matrix (ECM) remodeling and tissue fibrosis, and participate in the pathogenesis of asthma. In this study, the role of CD147 in airway remodeling and activation of circulating fibrocytes was investigated in asthmatic mice. Methods Asthmatic mouse model was established by sensitizing and challenging mice with ovalbumin (OVA), and treated with anti-CD147 or Isotype antibody. The number of eosinophils in bronchoalveolar lavage fluid (BALF) was examined by microscope, and the levels of interleukin-4 (IL-4), IL-5 and IL-13 in BALF were detected by enzyme-linked immunosorbent assay (ELISA). The number of CD45+ and collagen I (COL-I)+ circulating fibrocytes in BALF was detected by flow cytometry. Lung tissue sections were respectively stained with hematoxylin and eosin (HE), periodic acid-Schiff (PAS) or Masson trichrome staining, or used for immunohistochemistry of CD31 and immunohistofluorescence of α-smooth muscle actin (α-SMA), CD45 and COL-I. The protein expression of α-SMA, vascular endothelial growth factor (VEGF), transforming growth factor-β1 (TGF-β1), Fibronectin, and COL-I was determined by western blotting. Results Anti-CD147 treatment significantly reduced the number of eosinophils and the levels of IL-4, IL-13, and IL-5 in BALF, and repressed airway inflammatory infiltration and airway wall thickening in asthmatic mice. Anti-CD147 treatment also reduced airway goblet cell metaplasia, collagen deposition, and angiogenesis in asthmatic mice, accompanied by inhibition of VEGF and α-SMA expression. The number of CD45+COL-I+ circulating fibrocytes was increased in BALF and lung tissues of OVA-induced asthmatic mice, but was decreased by anti-CD147 treatment. In addition, anti-CD147 treatment also reduced the protein expression of COL-I, fibronectin, and TGF-β1 in lung tissues of asthmatic mice. Conclusion OVA-triggered airway inflammation and airway remodeling in asthmatic mice can be repressed by anti-CD147 treatment, along with inhibiting the accumulation and activation of circulating fibrocytes.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

CD147 induces asthmatic airway remodeling and activation of circulating fibrocytes in a mouse model of asthma

Li,

Cheng,

Guo

et al. 2024

Respir Res

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“…[18][19][20] A study by Toyoma et al even proved that inactivation of CXCR4 will inhibit invasion and migration of tumor cells in SCC hypopharynx. 21 Overexpression of CXCR4 is found in many malignancies. This is caused by CXCR4 upregulation by HIF-1α and HIF-2 secreted by malignant cells as a response to their increased oxygen demand.…”

Section: Discussionmentioning

confidence: 99%

Correlation of HIF-1α, CXCR4 and MMP13 Expression in Laryngeal Squamous Cell Carcinoma With Cervical Nodal Status

Etty Hary Kusumastuti,

Anny Setijo Rahaju,

Alphania Rahniayu

et al. 2021

Indian Journal of Forensic Medicine & Toxicology

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Background: Laryngeal carcinoma is the most common malignancy of the upper respiratory tract, more than 98% are squamous cell carcinoma (SCC). New method is necessary for identifying and predicting nodal metastasis in laryngeal SCC. Overproliferating tumor cells will induce hypoxia and release HIF-1α, which in turn will upregulate CXCR4. CXCR4 then will induce MMP13, a protein that degrade extracellular matrix (ECM), thus promoting metastatic process. Methods:A cross sectional study, using 30 samples of laryngeal SCC, divided into two groups: based on cervical lymph node status. All samples were stained immunohistochemically against HIF-1α, CXCR4 and MMP13 antibody. The expressions were evaluated using immunoreactive score (IRS).Result: There were significant difference among HIF1α, CXCR4, and MMP13 in laryngeal SCC with positive nodal metastasis group compared to negative nodal metastasis group (p<0,05). There was no significant correlation between HIF-1α expression and CXCR4 expression (p = 0,403) (p>0,05). There were significant correlation between HIF-1α and MMP13 expression (r s = 0,499), and between CXCR4 and MMP13 expression (r s = 0,409). Conclusion: There were significant differences in HIF-1α, CXCR4 and MMP13 immunoexpression in laryngeal SCC with cervical nodal metastasis compared to laryngeal SCC without cervical nodal metastasis. There was a positive correlation between HIF-1α and MMP13 expression, positive correlation between CXCR4 and MMP13 expression, but there was no correlation between HIF-1α and CXCR4 expression.

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N‐[4‐(Benzyloxy)‐3‐methoxybenzyl)]adamantane‐1‐amine (DZH2), a dual CCR5 and CXCR4 inhibitor as a potential agent against triple negative breast cancer

Rostom,

El‐Zohairy,

Marzouk

et al. 2024

Archiv der Pharmazie

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DZH2, a dual inhibitor of the chemokine receptors CCR5 and CXCR4, was discovered from virtual screening for CCR5 antagonists. In specific Ca2+ chemokine signaling assays, DZH2 displayed low micromolar IC50 values at both chemokine receptors. Its binding to intracellular allosteric binding sites of CCR5 and CXCR4 was confirmed by MD simulations and binding free‐energy calculations. DZH2 is superior to the CCR5 antagonist maraviroc in terms of its inhibitory activity on the growth of two breast cancer cell lines. In MCF7 and MDA‐MB‐231 cells, DZH2 was a >100‐fold more potent inhibitor of cell viability compared to maraviroc. DZH2 (6.7 µM) reduced migration of MDA‐MB‐231 cells to 4% compared to 50% inhibition of migration caused by maraviroc (780 µM). Also, DZH2 was a significantly more potent inhibitor of colony formation in MDA‐MB‐231 cells than maraviroc. In MCF10 cells, DZH2 caused no alteration in the gene expression with respect to cellular pathways mediating cell death, indicating its selectivity to breast cancer cells.

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SDF‑1/CXCR4 induces cell invasion through CD147 in squamous cell carcinoma of the hypopharynx

Cited by 6 publications

References 49 publications

CD147 induces asthmatic airway remodeling and activation of circulating fibrocytes in a mouse model of asthma

CD147 induces asthmatic airway remodeling and activation of circulating fibrocytes in a mouse model of asthma

Correlation of HIF-1α, CXCR4 and MMP13 Expression in Laryngeal Squamous Cell Carcinoma With Cervical Nodal Status

N‐[4‐(Benzyloxy)‐3‐methoxybenzyl)]adamantane‐1‐amine (DZH2), a dual CCR5 and CXCR4 inhibitor as a potential agent against triple negative breast cancer

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