Immunostaining of βA-Activin and Follistatin Is Decreased in HPV(+) Cervical Pre-Neoplastic and Neoplastic Lesions
Victor Jesus Huaringa Payano,
Lara Verônica de Araújo Lopes,
Larissa Rodrigues Peixoto,
Keila Alves da Silva,
Tania Maria Ortiga-Carvalho,
Alexandre Tafuri,
Annamaria Ravara Vago,
Enrrico Bloise
Affiliations
Victor Jesus Huaringa Payano
Laboratório de Patogênese Molecular, Departamento de Morfologia, Universidade Federal de Minas Gerais, Belo Horizonte 31270-910, MG, Brazil
Lara Verônica de Araújo Lopes
Laboratório de Patogênese Molecular, Departamento de Morfologia, Universidade Federal de Minas Gerais, Belo Horizonte 31270-910, MG, Brazil
Larissa Rodrigues Peixoto
Laboratório de Patogênese Molecular, Departamento de Morfologia, Universidade Federal de Minas Gerais, Belo Horizonte 31270-910, MG, Brazil
Keila Alves da Silva
Laboratório de Patogênese Molecular, Departamento de Morfologia, Universidade Federal de Minas Gerais, Belo Horizonte 31270-910, MG, Brazil
Tania Maria Ortiga-Carvalho
Laboratório de Endocrinologia Translacional, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro 21941-902, RJ, Brazil
Alexandre Tafuri
Laboratório de Anatomia Patológica Tafuri, Belo Horizonte 30170-133, MG, Brazil
Annamaria Ravara Vago
Laboratório de Patogênese Molecular, Departamento de Morfologia, Universidade Federal de Minas Gerais, Belo Horizonte 31270-910, MG, Brazil
Enrrico Bloise
Laboratório de Patogênese Molecular, Departamento de Morfologia, Universidade Federal de Minas Gerais, Belo Horizonte 31270-910, MG, Brazil
The activin–follistatin system regulates several cellular processes, including differentiation and tumorigenesis. We hypothesized that the immunostaining of βA-activin and follistatin varies in neoplastic cervical lesions. Cervical paraffin-embedded tissues from 162 patients sorted in control (n = 15), cervical intraepithelial neoplasia (CIN) grade 1 (n = 38), CIN2 (n = 37), CIN3 (n = 39), and squamous cell carcinoma (SCC; n = 33) groups were examined for βA-activin and follistatin immunostaining. Human papillomavirus (HPV) detection and genotyping were performed by PCR and immunohistochemistry. Sixteen samples were inconclusive for HPV detection. In total, 93% of the specimens exhibited HPV positivity, which increased with patient age. The most detected high-risk (HR)-HPV type was HPV16 (41.2%) followed by HPV18 (16%). The immunostaining of cytoplasmatic βA-activin and follistatin was higher than nuclear immunostaining in all cervical epithelium layers of the CIN1, CIN2, CIN3, and SCC groups. A significant decrease (p p < 0.05) in specific epithelial layers of cervical tissues from CIN1, CIN2, CIN3, and SCC compared to the control. Decreased immunostaining of cervical βA-activin and follistatin at specific stages of CIN progression suggests that the activin–follistatin system participates in the loss of the differentiation control of pre-neoplastic and neoplastic cervical specimens predominantly positive for HPV.
