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Updated: Jul 5, 2025

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Correlation of miR-155-5p, KRAS, and CREB Expression in Patients with Acute Myeloid Leukemia

Javad Garavand, Mohammad H Mohammadi, Mohammad T Jalali

    Clinical Laboratory
    |January 12, 2024
    PubMed
    Abstract

    Insights

    MicroRNA-155 (miR-155) and CREB are overexpressed in acute myeloid leukemia (AML). While miR-155 and CREB show increased expression in AML patients, KRAS does not, though CREB and KRAS correlate.

    Area of Science:

    • Molecular Biology
    • Oncology
    • Genetics

    Background:

    • Acute myeloid leukemia (AML) is a complex blood cancer characterized by genetic and microRNA (miRNA) aberrations.
    • MicroRNAs are key regulators in cancer development and progression.
    • This study investigates the interplay between miR-155, KRAS, and CREB in AML.

    Purpose of the Study:

    • To determine the expression levels of miR-155, KRAS, and CREB in AML patients compared to healthy controls.
    • To explore the correlation between these molecules and their potential impact on clinical parameters.
    • To elucidate the relationship between miR-155, KRAS, and CREB in the context of AML pathogenesis.

    Main Methods:

    • A case-control study involving 21 AML patients and 9 healthy controls.
    • Quantitative real-time PCR (RT-PCR) was utilized to measure the expression of miR-155, KRAS, and CREB.
    • Statistical analysis was performed using SPSS and GraphPad Prism software.

    Main Results:

    • miR-155 expression was significantly higher (35-fold) in AML patients versus controls (p < 0.0001).
    • CREB expression showed a 1.92-fold increase in AML patients (p = 0.034), while KRAS expression remained unchanged (p > 0.05).
    • A direct correlation was observed between CREB and KRAS expression (p = 0.0002), and both were linked to increased white blood cell counts.

    Conclusions:

    • miR-155 and CREB are significantly overexpressed in acute myeloid leukemia.
    • The findings highlight potential roles for miR-155 and CREB in AML development.
    • Further research is warranted to explore the therapeutic implications of targeting these molecules in AML.

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