IL-2 Induces Transient Arrest in the G1 Phase to Protect Cervical Cancer Cells from Entering Apoptosis

María Del Carmen Lagunas-Cruz; Arturo Valle-Mendiola; Jonathan Trejo-Huerta; Leticia Rocha-Zavaleta; María de Lourdes Mora-García; Adriana Gutiérrez-Hoya; Benny Weiss-Steider; Isabel Soto-Cruz

doi:10.1155/2019/7475295

IL-2 Induces Transient Arrest in the G1 Phase to Protect Cervical Cancer Cells from Entering Apoptosis

J Oncol. 2019 Sep 26:2019:7475295. doi: 10.1155/2019/7475295. eCollection 2019.

Authors

María Del Carmen Lagunas-Cruz¹, Arturo Valle-Mendiola¹, Jonathan Trejo-Huerta¹, Leticia Rocha-Zavaleta², María de Lourdes Mora-García¹, Adriana Gutiérrez-Hoya^{1

3}, Benny Weiss-Steider¹, Isabel Soto-Cruz¹

Affiliations

¹ Molecular Oncology Laboratory, Cell Differentiation and Cancer Research Unit, FES Zaragoza, National University of Mexico, Batalla 5 de Mayo S/n Col. Ejército de Oriente, CP 09230 Mexico City, Mexico.
² Department of Molecular Biology and Biotechnology, Institute of Biomedical Research, National University of Mexico, Mexico City, Mexico.
³ Cátedra CONACYT, CONACyT, Avenida Insurgentes Sur 1582, Col. Crédito Constructor Del. Benito Juárez, 03940 Mexico City, Mexico.

Abstract

Interleukin 2 (IL-2) has been used for the treatment of different types of cancer that express the IL-2 receptor (IL-2R). However, the effect of IL-2 on cervical cancer cells is unknown. IL-2R is present in normal cells of the immune system but not in the healthy cervix. We report that IL-2R is expressed in cervical cancer cells. IL-2 decreases cervical cancer cell proliferation via transient arrest of the G1 phase, which does not result in apoptosis or senescence. IL-2 upregulates the expression of p53 and p21 and downregulates cyclin D. In addition, we report the resistance of cervical cancer cells to treatments that induce apoptosis in HeLa and INBL cells. When arrested cells were treated with cisplatin, the cytokine protected cells from apoptosis induced by cisplatin. The effects of IL-2 on the cell cycle do not induce cellular senescence or activate the proapoptotic protein Bax. The cell arrest induced by IL-2 is conferring protection to cells against apoptosis.