PD-L1 inhibition with either PDL1Nb or PD-L1 mAb effectively represses MC-38 mouse sCRC tumour progression. (IMAGE)
Caption
(A) PDL1Nb, CTLA-4, Luc pDNA construction. (B) IB analysis shows the levels of PDL1Nb or CTLA-4Nb in the SFM of HEK293 cells transfected with PDL1Nb, CTLA-4Nb or Luc expression vectors. Mock: SFM. Positive control: a FLAG peptide, which was subsequently loaded on the SDS-PAGE gel (2) after the gel had run for a short time (1). (C) Schematic procedure of treatment of C57BL/6 mice bearing MC-38 mouse sCRC tumours treated with CTLA-4Nb-P, Luc-P or PDL1Nb-P via subcutaneous injection or intraperitoneal injection of PD-L1 mAb. Black arrows indicate treatments. (D) Treatment with either PD-L1 mAb or PDL1Nb-P, but not CTLA-4Nb-P, efficiently inhibited MC-38 tumour growth in mice (n=6–10). **p<0.01; ***p<0.001; two-tailed Student’s t-test. CTLA-4, cytotoxic T-lymphocyte-associated protein 4; CTLA-4Nb, CTLA-4 nanobody; CTLA-4Nb-P, CTLA-4Nb-plasmid construct; HEK293, human embryonic kidney 293 cells; IB, immunoblotting; Luc, luciferase; Luc-P, Luc-plasmid construct; mAb, monoclonal antibody; ns, not statistically significant; PD-1, programmed cell death protein 1; PD-L1, programmed death-ligand 1; PDL1Nb, PD-L1 nanobody; PDL1Nb-P, PD-L1Nb-plasmid construct; pDNA, plasmid DNA; SDS-PAGE, sodium dodecyl sulfate-polyacrylamide gel electrophoresis; sCRC, sporadic colorectal cancer; SFM, serum-free medium.
Credit
By Wen-Ming Chu, Li Ma, Brian Hew et al.
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