Annexin A1 peptide and endothelial cell-conditioned medium modulate cervical tumorigenesis
Cervical cancer is one of the leading causes of cancer death in women worldwide, and its tumorigenesis can be influenced by the microenvironment. The anti-inflammatory protein annexin A1 (ANXA1) has been reported to be associated with cancer progression and metastasis, suggesting that it plays a rol...
| Autores: | ; ; ; ; ; |
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| Tipo de documento: | Artículo |
| Estado: | Published version |
| Fecha de publicación: | 2019 |
| País: | Brasil |
| Institución: | UNESP |
| Repositorio: | Repositório Institucional da UNESP |
| Lenguaje: | Inglés |
| OAI Identifier: | oai:repositorio.unesp.br:11449/189701 |
| Acceso en línea: | http://dx.doi.org/10.1002/2211-5463.12603 http://hdl.handle.net/11449/189701 |
| Nivel de acceso: | Acceso abierto |
| Palabra clave: | ANXA1 carcinogenesis cervical cancer inflammation peptide treatment |
| Sumario: | Cervical cancer is one of the leading causes of cancer death in women worldwide, and its tumorigenesis can be influenced by the microenvironment. The anti-inflammatory protein annexin A1 (ANXA1) has been reported to be associated with cancer progression and metastasis, suggesting that it plays a role in regulating tumour cell proliferation. Here, we examined the effect of the N-terminal peptide Ac2-26 of ANXA1 on the HaCaT cell line (normal) and HeLa cell line (cervical cancer) co-cultured with endothelium cell-conditioned medium (HMC). Treatment with Ac2-26 decreased proliferation and increased motility of cervical cancer cells, but did not affect cellular morphology or viability. Combined HMC stimulus and Ac2-26 treatment resulted in an increase in apoptotic HeLa cells, upregulated expression of MMP2, and downregulated expression of COX2, EP3 and EP4. In conclusion, Ac2-26 treatment may modulate cellular and molecular mechanisms underlying cervical carcinogenesis. |
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