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B7H3与纤维连接蛋白相互作用对人慢性髓性白血病细胞凋亡影响的初步探讨
OBJECTIVE: To explore the effect of the interaction between B7H3 and fibronectin (FN) on the apoptosis of human chronic myeloid leukemia K562 cells. METHODS: The expression of B7H3 molecules in K562 cells was detected using flow cytometry and B7H3 overexpressing cells were constructed. The interacti...
Formato: | Online Artículo Texto |
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Lenguaje: | English |
Publicado: |
Editorial office of Chinese Journal of Hematology
2021
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8763590/ https://www.ncbi.nlm.nih.gov/pubmed/35045656 http://dx.doi.org/10.3760/cma.j.issn.0253-2727.2021.11.009 |
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collection | PubMed |
description | OBJECTIVE: To explore the effect of the interaction between B7H3 and fibronectin (FN) on the apoptosis of human chronic myeloid leukemia K562 cells. METHODS: The expression of B7H3 molecules in K562 cells was detected using flow cytometry and B7H3 overexpressing cells were constructed. The interaction between B7H3 and FN was detected using the co-immunoprecipitation technology. After adding exogenous FN, cell experiments were performed to detect changes in adhesion and cell apoptosis. The changes in apoptosis-related proteins and PI3K/AKT signaling pathway were detected using Western blot. RESULTS: The expression of B7H3 was low in K562, and the cell line K562 OE (overexpression)-B7H3 and the control cell line K562 NC (negative control)-B7H3 were obtained after lentivirus transfection. There is an interaction between B7H3 and FN (P=0.036), and this interaction promoted cell adhesion (P<0.05), inhibited cell apoptosis (P<0.05), and activated the PI3K/AKT signaling pathway (P<0.05). CONCLUSION: B7H3 interacts with FN to promote cell adhesion and may inhibit K562 cell apoptosis by activating the PI3K/AKT signaling pathway. |
format | Online Article Text |
id | pubmed-8763590 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Editorial office of Chinese Journal of Hematology |
record_format | MEDLINE/PubMed |
spelling | pubmed-87635902022-01-30 B7H3与纤维连接蛋白相互作用对人慢性髓性白血病细胞凋亡影响的初步探讨 Zhonghua Xue Ye Xue Za Zhi 论著 OBJECTIVE: To explore the effect of the interaction between B7H3 and fibronectin (FN) on the apoptosis of human chronic myeloid leukemia K562 cells. METHODS: The expression of B7H3 molecules in K562 cells was detected using flow cytometry and B7H3 overexpressing cells were constructed. The interaction between B7H3 and FN was detected using the co-immunoprecipitation technology. After adding exogenous FN, cell experiments were performed to detect changes in adhesion and cell apoptosis. The changes in apoptosis-related proteins and PI3K/AKT signaling pathway were detected using Western blot. RESULTS: The expression of B7H3 was low in K562, and the cell line K562 OE (overexpression)-B7H3 and the control cell line K562 NC (negative control)-B7H3 were obtained after lentivirus transfection. There is an interaction between B7H3 and FN (P=0.036), and this interaction promoted cell adhesion (P<0.05), inhibited cell apoptosis (P<0.05), and activated the PI3K/AKT signaling pathway (P<0.05). CONCLUSION: B7H3 interacts with FN to promote cell adhesion and may inhibit K562 cell apoptosis by activating the PI3K/AKT signaling pathway. Editorial office of Chinese Journal of Hematology 2021-11 /pmc/articles/PMC8763590/ /pubmed/35045656 http://dx.doi.org/10.3760/cma.j.issn.0253-2727.2021.11.009 Text en 2021年版权归中华医学会所有 https://creativecommons.org/licenses/by/3.0/This work is licensed under a Creative Commons Attribution 3.0 License. |
spellingShingle | 论著 B7H3与纤维连接蛋白相互作用对人慢性髓性白血病细胞凋亡影响的初步探讨 |
title | B7H3与纤维连接蛋白相互作用对人慢性髓性白血病细胞凋亡影响的初步探讨 |
title_full | B7H3与纤维连接蛋白相互作用对人慢性髓性白血病细胞凋亡影响的初步探讨 |
title_fullStr | B7H3与纤维连接蛋白相互作用对人慢性髓性白血病细胞凋亡影响的初步探讨 |
title_full_unstemmed | B7H3与纤维连接蛋白相互作用对人慢性髓性白血病细胞凋亡影响的初步探讨 |
title_short | B7H3与纤维连接蛋白相互作用对人慢性髓性白血病细胞凋亡影响的初步探讨 |
title_sort | b7h3与纤维连接蛋白相互作用对人慢性髓性白血病细胞凋亡影响的初步探讨 |
topic | 论著 |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8763590/ https://www.ncbi.nlm.nih.gov/pubmed/35045656 http://dx.doi.org/10.3760/cma.j.issn.0253-2727.2021.11.009 |
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