Blood: Prostatin E2 restores the sensitivity of leukemia cells to glucoscosteroids.

Glucocoderosterone (GC) resistance remains a clinical challenge for acute lymphoblastic leukemia (ALL) in children, and reactgenia to GC is a reliable predictive indicator.
to clarify the path of GC drug resistance, Roderic and others conducted survival-based genome-wide shRNA screening in mice with acute T lymphoblastic leukemia (T-ALL) cells.
finally identified genes that interfered with cAMP signaling and expressed the downward gene in GC-resistant or relapsed ALL patients (272 genes expressed downwards in patients with recurrent leukemia and 369 genes expressed significantly lower in GC drug-resistant patient samples).
whether in and out of the body, silent cAMP activation of the bird's bean nucleotide binding protein (alpha stimulation Gnas gene) can interfere with GC-induced gene expression, leading to dexamisone resistance.
researchers have confirmed that cAMP signaling and desemethone work together to increase the death of GC-resistant human T-ALL cells.
In addition, the researchers found that prostatin E recepposer 4 was expressed in T-ALL samples and demonstrated that prostin E2 (PGE2) increases in-cell cAMP, enhances GC-induced gene expression, and makes T-ALL samples sensitive to desermison.
findings suggest that PGE2 is the target for making recurrent children T-ALL more sensitive to GC.
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