Role of wnt ligand secretion mediator signaling in cancer development
Objective: The Wnt signaling pathway is among the crucial cascades that regulate development and homeostasis of tissue. Data Sources: Further, it is closely associated with different types of cancer, which includes glioma, breast, colorectal, lung, and prostate cancer, and hepatocellular carcinoma (...
Gespeichert in:
Veröffentlicht in: | Journal of cancer research and practice 2023-01, Vol.10 (1), p.1-10 |
---|---|
Hauptverfasser: | , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
Zusammenfassung: | Objective: The Wnt signaling pathway is among the crucial cascades that regulate development and homeostasis of tissue. Data Sources: Further, it is closely associated with different types of cancer, which includes glioma, breast, colorectal, lung, and prostate cancer, and hepatocellular carcinoma (HCC). The deviant activation or inhibition of Wnt signaling regulates cancer progression, thereby exerting oncogenic or tumorsuppressive effects that control the invasion, metastasis, and metabolism of cancer cell. Study Selection: In the Wnt secretory pathway, lipidmodified Wnt molecules interact with Wnt ligand secretion mediator (WLS), a Wnt cargo receptor. Moreover, they are directed to the plasma membrane and then secreted. Results: Loss of WLS function leads to the accumulation of Wnt in the endoplasmic reticulum (ER), leading to retrograde Golgi-ER transport and ER stress associated with the pathogenesis of several conditions, including early embryonic death, and developmental defects related to lymphopoiesis, neurogenesis, and osteogenesis in adults. Although there is substantial evidence, the regulatory mechanisms through which WLS controls cellular functions are not fully elucidated. Conclusion: Therefore, the current study aimed to identify the underlying mechanism of the effects of WLS on the development of human diseases. |
---|---|
ISSN: | 2311-3006 2311-3006 |
DOI: | 10.4103/ejcrp.eJCRP-D-22-00029 |