Long non-coding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1) is confirmed to be involved in regulation of the multiple myeloma (MM) process. However, its underlying molecular mechanism deserves further investigation.

Material and methods:
Quantitative real-time PCR was used to examine NEAT1, microRNA (miR)-133a and actin-related protein 2/3 complex subunit 5 (ARPC5) expression. Cell proliferation and apoptosis were evaluated by cell counting kit 8 assay, soft-agar colony formation assay and flow cytometry. Dual-luciferase reporter assay was used to confirm the interaction between miR-133a and NEAT1 or ARPC5. The localization of NEAT1 and miR-133a in MM cells was determined by fluorescent in situ hybridization assay. In addition, animal experiments were conducted to explore the effect of NEAT1 knockdown on MM tumor growth in vivo.

NEAT1 had increased expression in MM patients and cells. NEAT1 knockdown could repress MM cell proliferation and enhance apoptosis. NEAT1 could sponge miR-133a, and miR-133a could target ARPC5. MiR-133a was lowly expressed and ARPC5 was highly expressed in MM patients. MiR-133a inhibitor could abolish the suppressive effect of NEAT1 knockdown on MM cell growth, and these effects also could be reversed by ARPC5 silencing.

Animal experiments showed that NEAT1 downregulation reduced MM tumor growth by regulating miR-133a/ARPC5 axis. NEAT1 facilitated MM progression through the regulation of miR-133a/ARPC5, which provided new evidence that NEAT1 was a potential therapeutic target for MM.

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