Recurrence of cervical cancer and its resistance to progestin therapy in a mouse model

Fabiola F. Mehta; Seunghan Baik; Sang-Hyuk Chung

doi:10.18632/oncotarget.13676

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Research Papers:

Recurrence of cervical cancer and its resistance to progestin therapy in a mouse model

Fabiola F. Mehta, Seunghan Baik and Sang-Hyuk Chung _

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Oncotarget. 2017; 8:2372-2380. https://doi.org/10.18632/oncotarget.13676

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Abstract

Fabiola F. Mehta1, Seunghan Baik1, Sang-Hyuk Chung1

1Center for Nuclear Receptors and Cell Signaling, Department of Biology and Biochemistry, University of Houston, Houston, TX 77204, USA

Correspondence to:

Sang-Hyuk Chung, email: [email protected]

Keywords: cervical cancer, recurrence, therapy resistance, medroxyprogesterone acetate (MPA), human papillomavirus (HPV)

Received: May 23, 2016 Accepted: November 21, 2016 Published: November 29, 2016

ABSTRACT

Studies using K14E6/K14E7 transgenic mice expressing E6 and E7 oncoprotein of human papillomavirus type 16 (HPV16) have demonstrated that estrogen (E₂) is required for the genesis and growth of cervical cancer. Our prior study using the same mouse model has showed that progestin drug medroxyprogesterone acetate (MPA) promotes regression of primary cervical cancer. In the present study, we use the same transgenic mouse model to determine whether the cancer recurs after MPA therapy. Cervical cancer recurred even if MPA treatment was continued. Unlike primary cervical cancer, the cancer recurred even in the absence of exogenous E₂ when MPA treatment was ceased. Furthermore, recurrent cervical cancer did not fully regress upon MPA treatment. Our results support that MPA fails to completely eliminate primary cervical cancer cells and that remaining cancer cells grow independent of exogenous E₂ and are refractory to MPA.

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Research Papers:

Recurrence of cervical cancer and its resistance to progestin therapy in a mouse model

Abstract