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A Feedback Loop Between miR-30a/c-5p and DNMT1 Mediates Cisplatin Resistance in Ovarian Cancer Cells

Xi Han, Shuai Zhen, Zhongxue Ye

    Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology
    |February 22, 2017
    PubMed
    Abstract

    Insights

    Dysregulated miR-30a-5p and miR-30c-5p expression drives cisplatin resistance in ovarian cancer by impacting DNMT1 and Snail. Restoring these microRNAs may offer a new therapeutic strategy for ovarian cancer treatment.

    Area of Science:

    • Oncology
    • Molecular Biology
    • Epigenetics

    Background:

    • MicroRNAs (miRs) are implicated in cancer development and chemo-resistance.
    • Aberrant microRNA expression patterns are linked to chemo-resistance in cancer cells.
    • The role of miR-30 family members in cisplatin-resistance of ovarian cancer cells requires investigation.

    Purpose of the Study:

    • To investigate the role of miR-30 family members in cisplatin-resistance of ovarian cancer cells.
    • To elucidate the molecular mechanisms underlying miR-30a-5p and miR-30c-5p dysregulation in cisplatin-resistant ovarian cancer.
    • To explore the potential of targeting the miR-30a/c-5p and DNMT1 feedback loop for ovarian cancer therapy.

    Main Methods:

    • Quantitative reverse transcription PCR (qRT-PCR) for differential microRNA expression analysis.
    • Cell viability (CCK8 assay) and apoptosis (flow cytometry) assays to assess cisplatin sensitivity.
    • Western blotting and luciferase reporter assays to identify and validate microRNA targets.
    • Methylation-specific PCR to examine epigenetic regulation of microRNA precursors.

    Main Results:

    • miR-30a-5p and miR-30c-5p were significantly decreased in cisplatin-resistant ovarian cancer cells (CP70) compared to sensitive cells (A2780).
    • Overexpression of DNMT1 induced aberrant methylation, leading to decreased miR-30a-5p and miR-30c-5p levels.
    • miR-30a/c-5p directly targets and inhibits DNMT1 and Snail, key regulators of epithelial-mesenchymal transition (EMT).
    • Restoring miR-30a/c-5p or inhibiting DNMT1/Snail enhanced cisplatin sensitivity and partially reversed EMT in resistant cells.
    • Inhibiting miR-30a/c-5p or overexpressing DNMT1/Snail induced cisplatin resistance and partial EMT in sensitive cells.

    Conclusions:

    • A feedback loop between miR-30a/c-5p and DNMT1 is identified as a significant factor in cisplatin-resistance and EMT in ovarian cancer.
    • This miR-30a/c-5p/DNMT1 axis represents a promising therapeutic target for enhancing anti-cancer treatment efficacy in ovarian cancer.
    • Understanding this epigenetic regulatory network provides insights into overcoming chemo-resistance and managing ovarian cancer progression.
    Keywords:
    Cisplatin resistanceEpithelial-mesenchymal transitionMethylationOvarian cancermicroRNA

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