In vitro effects and mathematical modelling of CTCE‐9908 (a chemokine receptor 4 antagonist) on melanoma cell survival
CTCE‐9908, a CXC chemokine receptor 4 (CXCR4) antagonist, prevents CXCR4 phosphorylation and inhibits the interaction with chemokine ligand 12 (CXCL12) and downstream signalling pathways associated with metastasis. This study evaluated the in vitro effects of CTCE‐9908 on B16 F10 melanoma cells with...
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| Veröffentlicht in: | Clinical and experimental pharmacology & physiology 2024-06, Vol.51 (6), p.e13865-n/a |
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| creator | Basson, Charlise Phiri, Avulundiah Edwin Gandhi, Manjunath Anguelov, Roumen Serem, June Cheptoo Bipath, Priyesh Hlophe, Yvette Nkondo |
| description | CTCE‐9908, a CXC chemokine receptor 4 (CXCR4) antagonist, prevents CXCR4 phosphorylation and inhibits the interaction with chemokine ligand 12 (CXCL12) and downstream signalling pathways associated with metastasis. This study evaluated the in vitro effects of CTCE‐9908 on B16 F10 melanoma cells with the use of mathematical modelling. Crystal violet staining was used to construct a mathematical model of CTCE‐9908 B16 F10 (melanoma) and RAW 264.7 (non‐cancerous macrophage) cell lines on cell viability to predict the half‐maximal inhibitory concentration (IC50). Morphological changes were assessed using transmission electron microscopy. Flow cytometry was used to assess changes in cell cycle distribution, apoptosis via caspase‐3, cell survival via extracellular signal‐regulated kinase1/2 activation, CXCR4 activation and CXCL12 expression. Mathematical modelling predicted IC50 values from 0 to 100 h. At IC50, similar cytotoxicity between the two cell lines and ultrastructural morphological changes indicative of cell death were observed. At a concentration 10 times lower than IC50, CTCE‐9908 induced inhibition of cell survival (p = 0.0133) in B16 F10 cells but did not affect caspase‐3 or cell cycle distribution in either cell line. This study predicts CTCE‐9908 IC50 values at various time points using mathematical modelling, revealing cytotoxicity in melanoma and non‐cancerous cells. CTCE‐9908 significantly inhibited melanoma cell survival at a concentration 10 times lower than the IC50 in B16 F10 cells but not RAW 264.7 cells. However, CTCE‐9908 did not affect CXCR4 phosphorylation, apoptosis,\ or cell cycle distribution in either cell line. |
| doi_str_mv | 10.1111/1440-1681.13865 |
| format | Article |
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This study evaluated the in vitro effects of CTCE‐9908 on B16 F10 melanoma cells with the use of mathematical modelling. Crystal violet staining was used to construct a mathematical model of CTCE‐9908 B16 F10 (melanoma) and RAW 264.7 (non‐cancerous macrophage) cell lines on cell viability to predict the half‐maximal inhibitory concentration (IC50). Morphological changes were assessed using transmission electron microscopy. Flow cytometry was used to assess changes in cell cycle distribution, apoptosis via caspase‐3, cell survival via extracellular signal‐regulated kinase1/2 activation, CXCR4 activation and CXCL12 expression. Mathematical modelling predicted IC50 values from 0 to 100 h. At IC50, similar cytotoxicity between the two cell lines and ultrastructural morphological changes indicative of cell death were observed. At a concentration 10 times lower than IC50, CTCE‐9908 induced inhibition of cell survival (p = 0.0133) in B16 F10 cells but did not affect caspase‐3 or cell cycle distribution in either cell line. This study predicts CTCE‐9908 IC50 values at various time points using mathematical modelling, revealing cytotoxicity in melanoma and non‐cancerous cells. CTCE‐9908 significantly inhibited melanoma cell survival at a concentration 10 times lower than the IC50 in B16 F10 cells but not RAW 264.7 cells. However, CTCE‐9908 did not affect CXCR4 phosphorylation, apoptosis,\ or cell cycle distribution in either cell line.</description><identifier>ISSN: 0305-1870</identifier><identifier>EISSN: 1440-1681</identifier><identifier>DOI: 10.1111/1440-1681.13865</identifier><identifier>PMID: 38692577</identifier><language>eng</language><publisher>Australia: Wiley Subscription Services, Inc</publisher><subject>Animals ; Apoptosis ; Apoptosis - drug effects ; Caspase ; Cell cycle ; Cell Cycle - drug effects ; Cell death ; Cell Line, Tumor ; Cell lines ; Cell survival ; Cell Survival - drug effects ; Cell viability ; Chemokine CXCL12 - metabolism ; Chemokine receptors ; Chemokines ; CTCE‐9908 ; CXC chemokines ; CXCL12 ; CXCL12 protein ; CXCR4 ; CXCR4 protein ; Cytotoxicity ; Flow cytometry ; Gentian violet ; Macrophages ; mathematical modelling ; Mathematical models ; Melanoma ; Melanoma - drug therapy ; Melanoma - metabolism ; Melanoma - pathology ; Melanoma, Experimental - drug therapy ; Melanoma, Experimental - metabolism ; Melanoma, Experimental - pathology ; Metastases ; Mice ; Models, Biological ; Morphology ; Phosphorylation ; RAW 264.7 Cells ; Receptors, CXCR4 - antagonists & inhibitors ; Receptors, CXCR4 - metabolism ; Signal transduction ; Survival ; Toxicity ; Transmission electron microscopy</subject><ispartof>Clinical and experimental pharmacology & physiology, 2024-06, Vol.51 (6), p.e13865-n/a</ispartof><rights>2024 The Authors. published by John Wiley & Sons Australia, Ltd.</rights><rights>2024 The Authors. 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This study evaluated the in vitro effects of CTCE‐9908 on B16 F10 melanoma cells with the use of mathematical modelling. Crystal violet staining was used to construct a mathematical model of CTCE‐9908 B16 F10 (melanoma) and RAW 264.7 (non‐cancerous macrophage) cell lines on cell viability to predict the half‐maximal inhibitory concentration (IC50). Morphological changes were assessed using transmission electron microscopy. Flow cytometry was used to assess changes in cell cycle distribution, apoptosis via caspase‐3, cell survival via extracellular signal‐regulated kinase1/2 activation, CXCR4 activation and CXCL12 expression. Mathematical modelling predicted IC50 values from 0 to 100 h. At IC50, similar cytotoxicity between the two cell lines and ultrastructural morphological changes indicative of cell death were observed. At a concentration 10 times lower than IC50, CTCE‐9908 induced inhibition of cell survival (p = 0.0133) in B16 F10 cells but did not affect caspase‐3 or cell cycle distribution in either cell line. This study predicts CTCE‐9908 IC50 values at various time points using mathematical modelling, revealing cytotoxicity in melanoma and non‐cancerous cells. CTCE‐9908 significantly inhibited melanoma cell survival at a concentration 10 times lower than the IC50 in B16 F10 cells but not RAW 264.7 cells. However, CTCE‐9908 did not affect CXCR4 phosphorylation, apoptosis,\ or cell cycle distribution in either cell line.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Caspase</subject><subject>Cell cycle</subject><subject>Cell Cycle - drug effects</subject><subject>Cell death</subject><subject>Cell Line, Tumor</subject><subject>Cell lines</subject><subject>Cell survival</subject><subject>Cell Survival - drug effects</subject><subject>Cell viability</subject><subject>Chemokine CXCL12 - metabolism</subject><subject>Chemokine receptors</subject><subject>Chemokines</subject><subject>CTCE‐9908</subject><subject>CXC chemokines</subject><subject>CXCL12</subject><subject>CXCL12 protein</subject><subject>CXCR4</subject><subject>CXCR4 protein</subject><subject>Cytotoxicity</subject><subject>Flow cytometry</subject><subject>Gentian violet</subject><subject>Macrophages</subject><subject>mathematical modelling</subject><subject>Mathematical models</subject><subject>Melanoma</subject><subject>Melanoma - drug therapy</subject><subject>Melanoma - metabolism</subject><subject>Melanoma - pathology</subject><subject>Melanoma, Experimental - drug therapy</subject><subject>Melanoma, Experimental - metabolism</subject><subject>Melanoma, Experimental - pathology</subject><subject>Metastases</subject><subject>Mice</subject><subject>Models, Biological</subject><subject>Morphology</subject><subject>Phosphorylation</subject><subject>RAW 264.7 Cells</subject><subject>Receptors, CXCR4 - antagonists & inhibitors</subject><subject>Receptors, CXCR4 - metabolism</subject><subject>Signal transduction</subject><subject>Survival</subject><subject>Toxicity</subject><subject>Transmission electron microscopy</subject><issn>0305-1870</issn><issn>1440-1681</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><sourceid>EIF</sourceid><recordid>eNqFkc9u1DAQhy0EotvCmRuyxKU9pB3H8Z8cUbRApUpwKGfLiSclJbEXO9nSG4_AM_IkOGzpgQs-jKXRN59G8yPkFYNzlt8FqyoomNTsnHEtxROyeew8JRvgIAqmFRyR45RuAUCA5M_JUWbrUii1Id8vPd0PcwwU-x67OVHrHZ3s_AVzGTo70ik4HMfB39DQ0-a62f768bOuQdNTS7uMha-DRxqxw90cIq2yYbY3wQ9pPqPB0wlH68OU4ayhaYn7YW_HF-RZb8eELx_-E_L53fa6-VBcfXx_2by9KjoupShayaVDa2twjkGNJYDClnfKMYEOOQPOZSsciKqqdalLUFYw1cq20n1nNT8hpwfvLoZvC6bZTENaN7Eew5JMPhEwVWrFM_rmH_Q2LNHn7VaK63w8xTJ1caC6GFKK2JtdHCYb7w0Ds4Zi1gjMGoH5E0qeeP3gXdoJ3SP_N4UMiANwN4x4_z-fabafDuLfq9qVaw</recordid><startdate>202406</startdate><enddate>202406</enddate><creator>Basson, Charlise</creator><creator>Phiri, Avulundiah Edwin</creator><creator>Gandhi, Manjunath</creator><creator>Anguelov, Roumen</creator><creator>Serem, June Cheptoo</creator><creator>Bipath, Priyesh</creator><creator>Hlophe, Yvette Nkondo</creator><general>Wiley Subscription Services, Inc</general><scope>24P</scope><scope>WIN</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7TK</scope><scope>7U7</scope><scope>C1K</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-6123-9707</orcidid><orcidid>https://orcid.org/0000-0001-9912-166X</orcidid><orcidid>https://orcid.org/0000-0001-9794-5438</orcidid><orcidid>https://orcid.org/0000-0001-5456-0466</orcidid><orcidid>https://orcid.org/0000-0001-7291-1151</orcidid><orcidid>https://orcid.org/0000-0002-5433-7069</orcidid><orcidid>https://orcid.org/0000-0002-3112-2436</orcidid></search><sort><creationdate>202406</creationdate><title>In vitro effects and mathematical modelling of CTCE‐9908 (a chemokine receptor 4 antagonist) on melanoma cell survival</title><author>Basson, Charlise ; 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This study evaluated the in vitro effects of CTCE‐9908 on B16 F10 melanoma cells with the use of mathematical modelling. Crystal violet staining was used to construct a mathematical model of CTCE‐9908 B16 F10 (melanoma) and RAW 264.7 (non‐cancerous macrophage) cell lines on cell viability to predict the half‐maximal inhibitory concentration (IC50). Morphological changes were assessed using transmission electron microscopy. Flow cytometry was used to assess changes in cell cycle distribution, apoptosis via caspase‐3, cell survival via extracellular signal‐regulated kinase1/2 activation, CXCR4 activation and CXCL12 expression. Mathematical modelling predicted IC50 values from 0 to 100 h. At IC50, similar cytotoxicity between the two cell lines and ultrastructural morphological changes indicative of cell death were observed. At a concentration 10 times lower than IC50, CTCE‐9908 induced inhibition of cell survival (p = 0.0133) in B16 F10 cells but did not affect caspase‐3 or cell cycle distribution in either cell line. This study predicts CTCE‐9908 IC50 values at various time points using mathematical modelling, revealing cytotoxicity in melanoma and non‐cancerous cells. CTCE‐9908 significantly inhibited melanoma cell survival at a concentration 10 times lower than the IC50 in B16 F10 cells but not RAW 264.7 cells. 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| subjects | Animals Apoptosis Apoptosis - drug effects Caspase Cell cycle Cell Cycle - drug effects Cell death Cell Line, Tumor Cell lines Cell survival Cell Survival - drug effects Cell viability Chemokine CXCL12 - metabolism Chemokine receptors Chemokines CTCE‐9908 CXC chemokines CXCL12 CXCL12 protein CXCR4 CXCR4 protein Cytotoxicity Flow cytometry Gentian violet Macrophages mathematical modelling Mathematical models Melanoma Melanoma - drug therapy Melanoma - metabolism Melanoma - pathology Melanoma, Experimental - drug therapy Melanoma, Experimental - metabolism Melanoma, Experimental - pathology Metastases Mice Models, Biological Morphology Phosphorylation RAW 264.7 Cells Receptors, CXCR4 - antagonists & inhibitors Receptors, CXCR4 - metabolism Signal transduction Survival Toxicity Transmission electron microscopy |
| title | In vitro effects and mathematical modelling of CTCE‐9908 (a chemokine receptor 4 antagonist) on melanoma cell survival |
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