miR-30c-2-3p Regulates METTL14 Expression and Inhibits Cell Migration in Breast Cancer

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Emrence Z., Punar S., Zarerajabi V., Uslu S., Abaci N., Ekmekci S. S.

Curr. Issues Mol. Biol., cilt.48, sa.6, ss.1-10, 2026 (Scopus)

• Yayın Türü: Makale / Tam Makale
• Cilt numarası: 48 Sayı: 6
• Basım Tarihi: 2026
• Doi Numarası: 10.3390/cimb48060545
• Dergi Adı: Curr. Issues Mol. Biol.
• Derginin Tarandığı İndeksler: Scopus, PubMed
• Sayfa Sayıları: ss.1-10
• Açık Arşiv Koleksiyonu: AVESİS Açık Erişim Koleksiyonu
• İstanbul Üniversitesi Adresli: Evet

Özet

Abstract

Breast cancer remains a leading cause of cancer-related mortality worldwide, with epi-

genetic mechanisms like N6 methyladenosine (m6A) modification playing a crucial role

in tumorigenesis. The interaction between microRNAs and m6A regulators, such as the

methyltransferase METTL14, is increasingly recognized as a key pathway in oncogen-

esis. This study investigated whether miR-30c-2-3p regulates METTL14 expression to

influence global m6A levels and cell migration in breast epithelial (MCF12A) and breast

cancer (MCF7) cell lines. Following transfection with miR-30c-2-3p mimics, successful

overexpression was confirmed in both cell lines. Subsequent RT-qPCR and Western blotting

analyses demonstrated that METTL14 mRNA and protein levels were significantly reduced

at 24 and 48 h post-transfection (p < 0.05). Concurrently, global m6A RNA methylation

levels decreased, with a more pronounced reduction observed in MCF12A cells (p < 0.001).

Functionally, wound healing assays revealed that miR-30c-2-3p significantly inhibited

migration, reducing wound closure by 30–44% in MCF7 cells and by 66–72% in MCF12A

cells. These findings reveal a novel regulatory axis involving miR-30c-2-3p, METTL14,

and m6A, suggesting that miR-30c-2-3p functions as a tumor suppressor and represents a

promising biomarker and therapeutic target in breast cancer.