Knockdown of Beclin‐1 blocks NEK2‐mediated BTZ resistance in MM cells. (A) KMS11 EV + Scr, KMS11 EV + BECN1‐shRNA, KMS11 NEK2‐OE + Scr, KMS11 NEK2‐OE + BECN1‐shRNA MM cells were treated with BTZ (10 nm), cell viability was examined 48 h later. (B) RPMI 8226 EV + Scr, RPMI 8226 EV + BECN1‐shRNA, RPMI 8226 NEK2‐OE + Scr, RPMI 8226 NEK2‐OE + BECN1‐shRNA MM cells were treated with BTZ (10 nm), cell viability was examined 48 h later. (C) Clonogenic analysis of KMS11 EV + Scr, KMS11 EV + BECN1‐shRNA, KMS11 NEK2‐OE + Scr, KMS11 NEK2‐OE + BECN1‐shRNA MM cells after treatment with BTZ (1 nm), respectively (4×). (D) Clonogenic analysis of RPMI 8226 EV + Scr, RPMI 8226 EV + BECN1‐shRNA, RPMI 8226 NEK2‐OE + Scr, RPMI 8226 NEK2‐OE + BECN1‐shRNA MM cells after treatment with BTZ (1 nm), respectively (4×). (E) Assessment of apoptosis by using FITC‐Annexin V/PI staining in KMS11 NEK2‐OE + Scr, KMS11 NEK2‐OE + BECN1‐shRNA, RPMI 8226 NEK2‐OE + Scr, RPMI 8226 NEK2‐OE + BECN1‐shRNA MM cells after treatment with BTZ (10 nm). (F) Western blots of full‐length PARP, cleaved PARP, cleaved caspase‐3, NEK2, and β‐actin in KMS11 NEK2‐OE + Scr, KMS11 NEK2‐OE + BECN1‐shRNA, RPMI 8226 NEK2‐OE + Scr, RPMI 8226 NEK2‐OE + BECN1‐shRNA MM cells after treatment with BTZ (10 nm). *P < 0.05, **P < 0.01. Significance was determined by Student’s t‐test. Error bars indicate SD.