pd-1/pd-l1 interaction regulates bcl2, ki67, bax, and casp3, altering proliferation, survival, and apoptosis in acute myeloid leukemia

Programmed death ligand-1 (pd-l1) is a pivotal inhibitory checkpoint ligand known to induce t-cell exhaustion via interaction with the programmed death‑1 (pd‑1) receptor. beyond this, pd-l1’s intrinsic signaling pathways within cancer cells warrant further exploration. this study aims to elucidate the effect of pd-l1 stimulation on the proliferation, survival, and apoptosis of acute myeloid leukemia (aml) cell lines.two human aml cell lines, hl-60 and thp-1 were cultured and treated with phorbol 12-myristate 13-acetate (pma) to induce pd-l1overexpression. post-treatment pd-l1 expression was confirmed via flow cytometry. subsequently, cell surface pd-l1 was stimulated using a recombinant pd-1, 24 hours post-pma treatment. the expression alterations in pivotal genes including bcl2, mki67, bax, and casp3 were monitored using quantitative real-time polymerase chain reaction 24 and 48 hours post-treatment. additionally, annexin-v through flow cytometry.findings reveal that pd-l1 stimulation augments aml cell proliferation and survival by enhancing mki67 and bcl2 expressions while concurrently inhibiting cell apoptosis due to decreased bax and casp3 expression following pd-l1 stimulation. notably, stimulated cells expressed exhibited reduced annexin-v compared to control cells.this study underscores that pd-l1 stimulation fosters aml cell proliferation and survival while impeding cell apoptosis. the results hold potential implications for targeting pd-l1 in aml treatment strategies.