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A 60 kDa prolactin variant secreted by cervical cancer cells modulates apoptosis and cytokine production
Author(s) -
Adriï¿ ⁄ n Ramï¿ ⁄ rez De Arellano,
Annie Riera Leal,
Edgar Iván López-Pulido,
Luis Renee Gonzï¿ ⁄ lez-Lucano,
Josï¿ ⁄ Macï¿ ⁄ as Barragan,
Susana Del Toro Arreola,
Mariel Garcï¿ ⁄ a-Chagollan,
Claudia Palafox-Sï¿ ⁄ nchez,
Josï¿ ⁄ Muï¿ ⁄ oz-Valle,
Ana Laura Pereira-Suárez
Publication year - 2018
Publication title -
oncology reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.094
H-Index - 96
eISSN - 1791-2431
pISSN - 1021-335X
DOI - 10.3892/or.2018.6222
Subject(s) - apoptosis , cytokine , hela , cancer cell , oncogene , cancer research , tumor necrosis factor alpha , biology , cervical cancer , prolactin , cancer , cell growth , cell culture , cell , immunology , cell cycle , endocrinology , hormone , biochemistry , genetics
Prolactin (PRL) is associated with different types of cancer, such as cervical cancer. Recombinant PRL has antiapoptotic effect on cervical cancer cells, and it can also induce cytokine production on macrophages. A 60 kDa variant of PRL is produced by cervical cancer cells. The aim of the present study was to evaluate this variant's bioactivity, to test its effect on cervical cancer cell apoptosis, and to assess its ability to induce cytokine production on THP-1 macrophages. First, 60 kDa PRL was isolated and used to stimulate Nb2 cells. Later, apoptosis was measured after exposure to 60 kDa PRL. Finally, cytokines were measured on THP-1 stimulated supernatants. Our results show that 60 kDa PRL increased Nb2 cell proliferation. Apoptosis was decreased after stimuli with 60 kDa PRL in cervical cancer cells. IL-1β and TNF-α are produced by THP-1 macrophages after stimuli. These results suggest that 60 kDa PRL produced by cervical cancer cells is able to reduce apoptosis in HeLa, SiHa and C-33A cells and induce IL-1β and TNF-α production by THP-1 macrophages.

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