The relationship between beta-catenin and apoptosis: A cytological and immunocytochemical examination


DÖNMEZ H. G. , Demirezen S. , BEKSAÇ M. S.

TISSUE & CELL, cilt.48, ss.160-167, 2016 (SCI İndekslerine Giren Dergi) identifier identifier identifier

  • Cilt numarası: 48 Konu: 3
  • Basım Tarihi: 2016
  • Doi Numarası: 10.1016/j.tice.2016.04.001
  • Dergi Adı: TISSUE & CELL
  • Sayfa Sayıları: ss.160-167

Özet

Disruption of the adhesive role of beta-catenin by caspases has been reported; however, the relationship between the Wnt/beta-catenin signaling pathway and apoptosis remains unclear. Therefore, we aimed to evaluate squamous epithelial cells in cervicovaginal smears by using cytological and immunocytochemical methods to observe changes in the presence and localization of beta-catenin during apoptosis, death receptor-, and mitochondria-mediated apoptosis. We investigated 224 cervicovaginal smears using the Papanicolaou method. Anti-beta-catenin and anti-cleaved caspase 3, 8, and 9 antibodies were used for immunocytochemical staining. Apoptotic cells were negative for beta-catenin. This showed that the Wnt/beta-catenin signaling pathway was inactive in apoptotic cells. However, beta-catenin showed intense positivity in the membrane, cytoplasm, and nucleus of non-apoptotic epithelial cells around these apoptotic cells. Therefore, the Wnt/beta-catenin signaling pathway was active in non-apoptotic epithelial cells, and this activity in non-apoptotic cells may have been induced by apoptotic cells. A highly significant association between the presence of death receptor- mediated apoptosis and the activity of the Wnt/beta-catenin signaling pathway was also found (P < 0.001). In conclusion, the Wnt/beta-catenin signaling pathway was found to be inactive in apoptotic cells, but apoptotic cells may induce the Wnt/beta-catenin signaling pathway in non-apoptotic cells to compensate for a decrease in epithelial cells because of apoptosis in order to maintain epithelial tissue integrity. (C) 2016 Elsevier Ltd. All rights reserved.