Fig. 3

AHSA1 promotes MM proliferation and BTZ resistance through activating CDK6 and PSMD2 respectively. A-C Using Co-IP assay followed by MS, CDK6 and PSMD2 were selected among candidate genes of the proliferation-related and drug-resistance genes in ARP1 WT, AHSA1-OE cells, AHSA1-OE cells treated with Bufalin or BTZ, respectively. D WB analysis showed the expressions of CDK6 and PSMD2 in AHSA1-OE (Left) and AHSA1-KD cells (Right). E Co-IP experiment further confirmed the interaction between HSP90 with CDK6 and PSMD2 in ARP1 and H929 cells using HSP90 antibody as bait. F Co-IP experiment showed that CDK6 directly interacted with HSP90 in ARP1 and H929 cells. G Co-IP assay confirmed that PSMD2 interacted with HSP90 in ARP1 and H929 cells. H Proteasome activity assay showed that overexpression of AHSA1 in ARP1 and H929 cells resulting in high proteasome activity. I Validation of PSMD2 overexpression in ARP1 and H929 PSMD2-OE cells relative to WT cells. J Proteasome activity assay showed that overexpression of PSMD2 in ARP1 and H929 cells led to high proteasome activity. K-L Effects of BTZ on the cell viability of ARP1 (K) and H929 (L) cells with or without PSMD2 overexpression. The data are expressed as mean ± SD.*p<0.05, **p<0.01, ***p<0.001