AI Article Synopsis

  • MicroRNAs (miRNAs), particularly miR-204, are crucial in regulating gene expression and were studied for their impact on T-cell acute lymphoblastic leukaemia (T-ALL).
  • The study found that miR-204 was expressed at low levels in T-ALL, and increasing its expression inhibited cell proliferation, migration, and invasion in T-ALL cells.
  • Additionally, miR-204 was shown to directly bind to and inhibit SOX4, suggesting that it could be a promising therapeutic target for treating T-ALL.

Article Abstract

Background: MicroRNAs (miRNAs) are a group of small non-coding RNAs that play important roles in the pathogenesis of human diseases by negatively regulating gene expression. The aim of this study was to explore the effect of miR-204 on cell proliferation migration and invasion in T-cell acute lymphoblastic leukaemia (T-ALL).

Method: miR-204 expression was determined in bone marrow samples from 32 leukemia patients and 32 healthy controls by quantitative real-time PCR (qRT-PCR). The effect of miR-204 on cell proliferation was evaluated by CCK8 assay, cell migration and invasion were evaluated by transwell migration and invasion assays, In addition, the regulation of SOX4 by miR-204 was evaluated by luciferase reporter assay and western blot.

Results: our results revealed that miR-204 was low expressed in T-ALL. Cell proliferation assay showed that the cell proliferation ability was inhibited by miR-204 mimics. Moreover, migration and invasion assay suggested that overexpression of miR-204 could significantly suppressed the migration and invasion ability of T-ALL cells. Luciferase reporter assay confirmed that miR-204 directly bound to the 3' untranslated region of SOX4, and western blot suggested that miR-204 inhibited the expression of SOX4 at the protein levels.

Conclusions: Our findings indicated that miR-204 negatively regulates SOX4 and inhibited proliferation, migration and invasion of T-ALL cell lines. Thus, miR-204 might represent a potential therapeutic target for T-ALL intervention.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4583897PMC

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