USO1 promotes tumor progression via activating Erk pathway in multiple myeloma cells.

Biomed Pharmacother

Department of Hematology, Shanghai Pudong Hospital Affiliated to Fudan University, Shanghai 201399, China. Electronic address:

Published: March 2016

AI Article Synopsis

  • This study investigates how the gene USO1 affects the growth and death of multiple myeloma (MM) cells and looks into the underlying molecular mechanisms.
  • Researchers measured levels of USO1 and another protein called MIF in MM samples versus normal tissues, and assessed how knocking down USO1 impacted cell growth and apoptosis.
  • Findings revealed that higher USO1 and MIF levels in MM cells promote proliferation, while reducing USO1 leads to decreased growth and increased apoptosis, suggesting that USO1 could be a potential target for MM treatment and diagnosis.

Article Abstract

Objective: This study aimed to explore the influence of USO1 on multiple myeloma (MM) cell proliferation and apoptosis and the related molecular mechanism.

Methods: The expression of USO1 and MIF in MM tissues and cells, normal bone marrow tissues and cells were determined by qRT-PCR and western blot assay. The cell proliferation and apoptosis of MM cells before and after knockdown of USO1 were determined by MTT assay and flow cytometry, respectively. Before and after knockdown of USO1, the expression of the proliferation-related genes cyclin D1, Mcm2 and PCNA in MM cells was determined by qRT-PCR and western blot assay. The protein level of p-Erk1/2 and MIF was determined by western blot assay and ELISA, respectively.

Results: The expression levels of USO1 and MIF in MM tissues and cells were much higher than those in normal bone marrow tissues and cells. Knockdown of USO1 resulted in the inhibited ability of cell proliferation and induced cell apoptosis. The expression of cyclin D1, Mcm2, PCNA and p-Erk1/2 decreased significantly after knockdown of USO1 as well as the decreased MIF secretion.

Conclusion: USO1 gene may be a promising target for the therapy of human MM and its diagnosis marker.

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Source
http://dx.doi.org/10.1016/j.biopha.2016.01.012DOI Listing

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