TY - JOUR
T1 - VAV3 in human cancers
T2 - Mechanism and clinical implication
AU - Al-Hawary, Sulieman Ibraheem Shelash
AU - Alsalamy, Ali
AU - Gupta, Reena
AU - Alsaab, Hashem O.
AU - Hjazi, Ahmed
AU - Edilboyev, Unarbek
AU - Ramadan, Montather F.
AU - Hussien, Beneen M.
AU - Ahmed, Muhja
AU - Hosseini-Fard, Seyed Reza
N1 - Publisher Copyright:
© 2023 Elsevier GmbH
PY - 2023/8
Y1 - 2023/8
N2 - 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.
AB - 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.
KW - Biomarker
KW - Cancer
KW - GEF
KW - VAV3
UR - https://www.scopus.com/pages/publications/85165263882
U2 - 10.1016/j.prp.2023.154681
DO - 10.1016/j.prp.2023.154681
M3 - Review article
C2 - 37467637
AN - SCOPUS:85165263882
SN - 0344-0338
VL - 248
JO - Pathology Research and Practice
JF - Pathology Research and Practice
M1 - 154681
ER -
