CNS neuroscience & therapeutics · 2024
Phosphorylation of PBK at Thr9 by CDK5 correlates with invasion of prolactinomas.
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Fang Qiuyue, Liu Changxiaofeng, Nie Ding, Guo Jing, Xie Weiyan, Zhang Yazhuo
Аннотация
CONTEXT: Prolactinomas are the most prevalent functional pituitary neuroendocrine tumors (PitNETs), and they are invasive to surrounding anatomic structures. The detailed mechanisms of invasion are not yet clear.
OBJECTIVE: We explored the role of PBK phosphorylation in the proliferation and invasion of prolactinomas and its possible mechanism.
RESULTS: We report that PBK directly binds to and is phosphorylated at Thr9 by cyclin-dependent kinase 5 (CDK5), which promotes GH3 cell EMT progression and proliferation. Phosphorylation of PBK at Thr9 (pPBK-T9) by CDK5 enhances the stability of PBK. p38 is one of the downstream targets of PBK, and its phosphorylation is reduced as pPBK-T9 increases in vivo and in vitro. Furthermore, we found that pPBK-T9 is highly expressed in invasive PitNETs and was significantly correlated with invasion by univariate and multivariate analyses.
CONCLUSIONS: Phosphorylation of PBK at Thr9 by CDK5 promotes cell proliferation and EMT progression in prolactinomas.
OBJECTIVE: We explored the role of PBK phosphorylation in the proliferation and invasion of prolactinomas and its possible mechanism.
RESULTS: We report that PBK directly binds to and is phosphorylated at Thr9 by cyclin-dependent kinase 5 (CDK5), which promotes GH3 cell EMT progression and proliferation. Phosphorylation of PBK at Thr9 (pPBK-T9) by CDK5 enhances the stability of PBK. p38 is one of the downstream targets of PBK, and its phosphorylation is reduced as pPBK-T9 increases in vivo and in vitro. Furthermore, we found that pPBK-T9 is highly expressed in invasive PitNETs and was significantly correlated with invasion by univariate and multivariate analyses.
CONCLUSIONS: Phosphorylation of PBK at Thr9 by CDK5 promotes cell proliferation and EMT progression in prolactinomas.