Journal
FRONTIERS IN ONCOLOGY
Volume 11, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fonc.2021.668617
Keywords
Mantle cell lymphoma; G protein-coupled estrogen receptor (GPER); G-1; cell proliferation; apoptosis; chemotherapy-free strategies
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Funding
- National Natural Science Foundation of China [81828001, 81702641]
- Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD)
- Jiangxi Science Fund for Distinguished Young Scholars [2018ACB21042]
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Research shows that activation of GPER with selective agonist G-1 can induce cell cycle arrest, DNA damage, and apoptosis of MCL cell lines, as well as inhibit MCL cell proliferation, exhibiting anti-tumor functions. Combined use with ibrutinib has a synergistic effect, making it a potential candidate for chemotherapy-free therapies against MCL.
Mantle cell lymphoma (MCL) is an aggressive form of non-Hodgkin's B-cell lymphoma with poor prognosis. Despite recent advances, resistance to therapy and relapse remain significant clinical problems. G-protein-coupled estrogen receptor (GPER)-mediated estrogenic rapid signaling is implicated in the development of many cancers. However, its role in MCL is unknown. Here we report that GPER activation with selective agonist G-1 induced cell cycle arrest, DNA damage, mitochondria membrane potential abnormality, and eventually apoptosis of MCL cell lines. We found that G-1 induced DNA damage and apoptosis of MCL cells by promoting the expression of nicotinamide adenine dinucleotide phosphate oxidase and the generation of reactive oxygen species. In addition, G-1 inhibited MCL cell proliferation by inactivation of NF-kappa B signaling and exhibited anti-tumor functions in MCL xenografted mice. Most significantly, G-1 showed synergistic effect with ibrutinib making it a potential candidate for chemotherapy-free therapies against MCL.
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