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Turkish Journal of Biology

DOI

10.3906/biy-0904-24

Abstract

The Wnt signaling pathway is evolutionary conserved and controls many biological processes like cell proliferation and differentiation. It also provides planar polarity, regulation of the cell cycle, and cell adhesion during both the embryonic and adult period. However, it has been widely considered in the literature that some pathological alterations in various biomolecules involved in this pathway, and aberrant activation of signaling have important roles primarily in the genesis of colorectal and cervical cancer and several other serious diseases. The Wnt signaling pathway diversifies into 3 types: Wnt\beta-catenin signaling pathway, planar cell polarity pathway, and Wnt/calcium (Ca^{+2}) pathway. Only the Wnt\beta -catenin signaling pathway is dealt with in our review, because of its close relation with diseases. In recent years, numerous studies about the Wnt\beta -catenin signaling pathway have led to an explanation of the signal mechanism and the identification of all components and the relation with the other signaling pathways. All of these studies have provided crucial contributions to novel diagnostic and therapeutic methods. Gynecological cancers originate in the female reproductive organs and include cervical, endometrium, ovarian, vulvar, and fallopian cancers. These cancers are very significant because they are seen in about 45% of women. The most common type of gynecological malignancies are cervical and ovarian cancers, and their progression may result in death, and so clarifying the mechanisms of carcinogenesis is very important for producing new targets for therapy methods. Thus, in our review, it is planned to explain the relation of gynecological cancers, whose mortality is the highest after breast cancer in Turkey and worldwide, with the Wnt\beta -catenin signaling pathway and its biomolecules in the light of the literature.

Keywords

Wnt\beta -catenin signaling pathway, cancer, \beta -catenin, adhesion, cell proliferation

First Page

227

Last Page

234

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