PCSK1N as a Tumor Size Marker and an Endoplasmic Reticulum (ER) Stress Response Protein in Corticotroph Pituitary Adenomas
Authors' conclusion
PCSK1N is higher in SCA compared with FCA, and associated with corticotroph cell markers and tumor size. PCSK1N is likely to be part of the adaptive response to ER stress, potentially conferring a survival advantage to the corticotroph tumor cell in conjunction with other proteins.
Study context
- Population
- Patients with corticotroph pituitary adenomas; mouse pituitary corticotroph tumor (AtT-20) cells
- Comparison
- Functioning (FCA) vs silent corticotroph adenomas (silent corticotroph adenoma (SCA)); 17-AAG-induced ER stress in AtT-20 cells
- Outcome
- Gene expression in adenoma tissue
Methodological detailscross-sectional tissue gene expression analysis, in vitro AtT-20 cell model
- Cross-sectional tissue gene expression analysis
- In vitro AtT-20 cell model
Main finding
As reported in the abstract
PCSK1N correlation with pro-opiomelanocortin (POMC), all CA
rs = −0.514
P < .001
PCSK1N correlation with TPIT, all CA
rs = −0.386
P = .005
PCSK1N correlation with PCSK1, all CA
rs = −0.3691
P = .008
PCSK1N correlation with tumor largest diameter, all CA
rs = 0.645
P < .001
Further findings
ER stress induced by 17-AAG in AtT-20 cells · 24 hours
- Decrease of Pomc and increase of Pcsk1n gene expression
- Downregulation of cell cycle, apoptosis and senescence pathways, and altered cell adhesion and cytoskeleton at protein level
Parts of this Brief are withheld: the automatic checks could not confirm them against the abstract.
Original publication
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