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Inhibiting MAPK14 showed anti-prolactinoma effect
Qiao-Yan Ding1,2,3, Yu Zhang3, Li Ma1,2
1Central lab, Tongren Hospital Affiliated to Wuhan University, The Third Hospital of Wuhan, 241 Pengliuyang Road, Wuchang District, Wuhan, 430060, Hubei, China.
BMC Endocrine Disorders
|September 7, 2020
Summary
p38 mitogen-activated protein kinase 14 (MAPK14) promotes prolactinoma formation by increasing prolactin (PRL) expression. Inhibiting MAPK14 may offer a new therapeutic strategy for treating prolactinoma.
Area of Science:
- Endocrinology
- Molecular Biology
- Oncology
Background:
- The pathogenesis of prolactinoma remains unclear.
- p38 mitogen-activated protein kinase (MAPK) signaling pathways are implicated in various cancers.
Purpose of the Study:
- To investigate the role of MAPK14 in prolactinoma development.
- To explore MAPK14 as a potential therapeutic target for prolactinoma.
Main Methods:
- Immunofluorescence analysis of prolactin (PRL) and MAPK14 expression in mouse and human prolactinoma tissues.
- Utilized estradiol-induced and dopamine D2 receptor knockout (DRD2-/-) mouse models with varying MAPK14 genotypes.
- Employed small interfering RNA (siRNA) to inhibit MAPK14 expression in GH3 cells.
Main Results:
- PRL and MAPK14 expression were co-localized and elevated in prolactinoma tissues.
- MAPK14 knockout significantly reduced tumor overgrowth and PRL expression in mouse models.
- siRNA-mediated MAPK14 inhibition decreased PRL production in GH3 cells.
Conclusions:
- MAPK14 plays a promoting role in prolactinoma formation.
- MAPK14 represents a potential therapeutic target for prolactinoma treatment.
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