Dergi
Molecular Cancer
Cilt
25
ISSN
14764598
Yayın Tarihi
1 Aralık 2026
Following publication of the original article [1], the authors identified two errors in Fig. 5, specifically: Fig. 5B: one incorrect image was misused. Fig. 5E: one incorrect image was misused. The corrected figures are provided below. The authors provided the Journal with the original data file. The correction does not affect the results or conclusions of the paper. The corrected Fig. 5B is presented below. The corrected Fig. 5E is presented below. The corrected Fig. 5 is presented below. CHEK1 induces macrophage osteoclasts by upregulating NFATc1 expression. A Magnetic resonance imaging (MRI) revealed that increased CHEK1 expression was positively correlated with bone lesion formation in the TT2 cohort MM patients. B–C TRAP staining revealed that Chek1 OE promoted osteoclast differentiation in RAW 264.7 mouse macrophages co-treated with RANKL (50 ng/mL) and M-CSF (15 ng/mL) in a time-dependent manner. D–E TRAP staining confirmed that Chek1 OE prompted osteoclast differentiation in RAW 264.7 cells treated with varying doses of RANKL and M-CSF in a manner dependent on RANKL and M-CSF dosages. F–G TRAP staining revealed that human primary peripheral blood mononuclear cells (PBMCs) transfected with human CHEK1 cDNA developed significantly more osteoclasts than non-transfected control cells. H–I Western blotting and TRAP staining confirmed that the CHEK1 inhibitor LY2603618 decreased NFATc1 expression and suppressed osteoclast differentiation in RAW 264.7 cells. J Co-IP revealed that CHEK1 interacted with NFATc1 in RAW 264.7 cells. K Western blotting confirmed that the expression of NFATc1 was increased in Chek1-OE RAW 264.7 cells relative to WT cells. L CHEK1 knockdown prevented myeloma-associated bone loss in the 5TMM3VT model. Micro-CT analysis of tibiae from 5TMM3VT mice at 4 weeks post-inoculation revealed osteolytic lesions and significantly reduced trabecular bone volume (BV/TV) compared with CHEK1-knockdown mice