Oncogenic signaling-mediated regulation of chromatin during tumorigenesis

• Published in: Cancer and metastasis reviews Vol. 42; no. 2; pp. 409 - 425
• Main Authors: Alam, Jahangir, Huda, Md Nazmul, Tackett, Alan J, Miah, Sayem
• Format: Journal Article
• Language: English
• Published: New York Springer US 01.06.2023; Springer; Springer Nature B.V
• Subjects: 1-Phosphatidylinositol 3-kinase; AKT protein; Apoptosis; Biomedical and Life Sciences; Biomedicine; Cancer; Cancer Research; Carcinogenesis - genetics; Carcinogenesis - metabolism; Cell cycle; Cell growth; Cell Transformation, Neoplastic - genetics; Cellular signal transduction; Chromatin; Chromatin - genetics; Development and progression; Environmental effects; Epigenetics; Gene expression; Genes; Homeostasis; Humans; Kinases; Ligands; Metastases; Metastasis; Oncology; Pathogenesis; Phosphatidylinositol 3-Kinases - metabolism; Phosphorylation; Physiology; Proteins; Signal transduction; Transcription factors; Transforming growth factor-b; Transforming growth factors; Tumorigenesis; Wnt protein; Wnt Signaling Pathway; Epigenetics; Signaling; Carcinogenesis and metastasis
• ISSN: 0167-7659; 1573-7233
• DOI: 10.1007/s10555-023-10104-3

Signaling pathways play critical roles in executing and controlling important biological processes within cells. Cells/organisms trigger appropriate signal transduction pathways in order to turn on or off intracellular gene expression in response to environmental stimuli. An orchestrated regulation of different signaling pathways across different organs and tissues is the basis of many important biological functions. Presumably, any malfunctions or dysregulation of these signaling pathways contribute to the pathogenesis of disease, particularly cancer. In this review, we discuss how the dysregulation of signaling pathways (TGF-β signaling, Hippo signaling, Wnt signaling, Notch signaling, and PI3K-AKT signaling) modulates chromatin modifications to regulate the epigenome, thereby contributing to tumorigenesis and metastasis.