AI Article Synopsis
- This study investigates the effects of methionine enkephalin (menk) on cervical cancer cell invasion, migration, and natural killer (NK) cell activation within the tumor microenvironment.
- Results indicate that menk inhibits the migration and invasion of cervical cancer cells by influencing epithelial to mesenchymal transition (EMT) markers, specifically increasing E-cadherin while decreasing N-cadherin and vimentin levels.
- In mouse models, menk was shown to enhance expression of certain NK cell markers (IFNγ and NKP46) in tumor tissues while reducing LAG3, suggesting that menk could be a promising avenue for future cervical cancer treatments.
Article Abstract
This study was to study the role of methionine enkephalin (menk) in cell invasion and migration as well as NK cells activation of tumor microenvironment in cervical cancer. The results showed that menk inhibited cervical cancer migration and invasion. In addition, we found menk affected epithelial to mesenchymal transition (EMT) related indicators, with increasing E-cadherin level, decreasing N-cadherin and vimentin level. Through in vivo mouse model, we found that menk IFNγ and NKP46 expression was upregulated in tumor tissues by menk compared with controls, while LAG3 expression was inhibited by menk, besides, there was an upregulation of CD11b NCR1 NKs of tumor microenvironment in cervical cancer. Therefore, we concluded that menk inhibited cancer migration and invasion via affecting EMT related indicators and activated CD11b NCR1 NKs of tumor microenvironment in cervical cancer, laying a theoretical foundation for the further clinical treatment of menk.
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| http://dx.doi.org/10.1016/j.intimp.2023.110967 | DOI Listing |
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