Your browser doesn't support javascript.
loading
Role of Transcription Factor BEND3 and Its Potential Effect on Cancer Progression.
Naiyer, Sarah; Dwivedi, Lalita; Singh, Nishant; Phulera, Swastik; Mohan, Vijay; Kamran, Mohammad.
Afiliação
  • Naiyer S; Department of Biomedical Science, University of Pennsylvania, Philadelphia, PA 19104, USA.
  • Dwivedi L; Faculty of Science, Department of Biotechnology, Invertis University, Bareilly 243122, UP, India.
  • Singh N; Cell and Gene Therapy Division Absorption System, Exton, PA 19341, USA.
  • Phulera S; Initium Therapeutics, 22 Strathmore Rd., STE 453, Natick, MA 01760, USA.
  • Mohan V; Department of Biosciences, School of Basic and Applied Sciences, Galgotias University, Greater Noida 203201, UP, India.
  • Kamran M; Department of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, NY 10065, USA.
Cancers (Basel) ; 15(14)2023 Jul 20.
Article em En | MEDLINE | ID: mdl-37509346
ABSTRACT
BEND3 is a transcription factor that plays a critical role in the regulation of gene expression in mammals. While there is limited research on the role of BEND3 as a tumor suppressor or an oncogene and its potential role in cancer therapy is still emerging, several studies suggest that it may be involved in both the processes. Its interaction and regulation with multiple other factors via p21 have already been reported to play a significant role in cancer development, which serves as an indication of its potential role in oncogenesis. Its interaction with chromatin modifiers such as NuRD and NoRC and its role in the recruitment of polycomb repressive complex 2 (PRC2) are some of the additional events indicative of its potential role in cancer development. Moreover, a few recent studies indicate BEND3 as a potential target for cancer therapy. Since the specific mechanisms by which BEND3 may contribute to cancer progression are not yet fully elucidated, in this review, we have discussed the possible pathways BEND3 may take to serve as an oncogenic driver or suppressor.
Palavras-chave

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Ano de publicação: 2023 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Ano de publicação: 2023 Tipo de documento: Article