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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