AI Article Synopsis
- GEFs are key players in cell signaling, facilitating the exchange of GDP for GTP which activates downstream effectors like Rho GTPase.
- The VAV GEF family, especially VAV3, acts as a molecular switch in signaling and is linked to cancer progression through its ability to promote various cancer-related processes like cell proliferation and migration.
- Research aims to uncover the mechanisms behind VAV3's role in cancers and evaluate its potential as a biomarker and mediator of resistance to cancer treatments.
Article Abstract
Guanine nucleotide exchange factors (GEFs) are primarily involved in signal transmission between cell membrane receptors and intracellular mediators. Upon replacing GDP with GTP, GEFs can alter their conformation, resulting in their binding to downstream effectors, such as GTPases like Ras homologous (Rho). VAV GEF family are versatile proteins working as an adaptor mediator and GEF for Rho GTPase. They act as a phosphorylation-dependent molecular switcher, fluctuating between active (tyrosine phosphorylated) and inactive (non-phosphorylated) conformation in cell signaling. Accumulating data showed that VAV3 is implicated in cancer progression. The higher levels of VAV3 in human cancers proposed that it may have an oncogenic role in cancer progression. Available studies demonstrated that VAV3 promoted cell proliferation, epithelial-mesenchymal transition (EMT), colony formation, cell cycle, survival, migration and invasion, and suppressed cell apoptosis. In addition, other studies indicated that VAV3 may have a prognostic value in cancer as well as it may act as a mediator in cancer chemoresistance. Here, we aimed to investigate the underlying molecular mechanism of VAV3 in cancer progression as well as to review its value as a prognostic biomarker and chemoresistance mediator in human cancers.
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| http://dx.doi.org/10.1016/j.prp.2023.154681 | DOI Listing |
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