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Author Lu, Yinghao ♦ Wu, Depei ♦ Wang, Jishi ♦ Li, Yan ♦ Chai, Xiao ♦ Kang, Qian
Source United States Department of Energy Office of Scientific and Technical Information
Content type Text
Language English
Subject Keyword APPLIED LIFE SCIENCES ♦ APOPTOSIS ♦ CELL PROLIFERATION ♦ DRUGS ♦ IN VITRO ♦ IN VIVO ♦ INHIBITION ♦ LEUKEMIA ♦ MICE ♦ THERAPY ♦ TRANSCRIPTION ♦ TRANSCRIPTION FACTORS
Abstract Aberrant expression of microRNAs (miRNAs) is implicated in cancer development and progression. While miR-320a is reported to be deregulated in many malignancy types, its biological role in multiple myeloma (MM) remains unclear. Here, we observed reduced expression of miR-320a in MM samples and cell lines. Ectopic expression of miR-320a dramatically suppressed cell viability and clonogenicity and induced apoptosis in vitro. Mechanistic investigation led to the identification of Pre-B-cellleukemia transcription factor 3 (PBX3) as a novel and direct downstream target of miR-320a. Interestingly, reintroduction of PBX3 abrogated miR-320a-induced MM cell growth inhibition and apoptosis. In a mouse xenograft model, miR-320a overexpression inhibited tumorigenicity and promoted apoptosis. Our findings collectively indicate that miR-320a inhibits cell proliferation and induces apoptosis in MM cells by directly targeting PBX3, supporting its utility as a novel and potential therapeutic agent for miRNA-based MM therapy. -- Highlights: •Expression of miR-320a in MM cell induces apoptosis in vitro. •miR-320a represses PBX3 via targeting specific sequences in the 3′UTR region. •Exogenous expression of PBX3 reverses the effects of miR-320a in inhibiting MM cell growth and promoting apoptosis. •Overexpression of miR-320a inhibits tumor growth and increases apoptosis in vivo.
ISSN 0006291X
Educational Use Research
Learning Resource Type Article
Publisher Date 2016-05-13
Publisher Place United States
Journal Biochemical and Biophysical Research Communications
Volume Number 473
Issue Number 4


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