Open AccessAnnexin A1 peptide and endothelial cell‐conditioned medium modulate cervical tumorigenesis
Author(s) -
Cardin Laila Toniol,
Prates Janesly,
Cunha Bianca Rodrigues,
Tajara Eloiza Helena,
Oliani Sonia Maria,
RodriguesLisoni Flávia Cristina
Publication year - 2019
Publication title -
febs open bio
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.718
H-Index - 31
ISSN - 2211-5463
DOI - 10.1002/2211-5463.12603
Subject(s) - hacat , carcinogenesis , hela , cancer research , cell growth , motility , apoptosis , annexin , cancer cell , cell , cell migration , cell culture , microbiology and biotechnology , metastasis , biology , cervical cancer , chemistry , cancer , biochemistry , genetics
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 ( ANXA 1) 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 ANXA 1 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 MMP 2 , and downregulated expression of COX 2 , EP 3 and EP 4 . In conclusion, Ac2‐26 treatment may modulate cellular and molecular mechanisms underlying cervical carcinogenesis.