miR-543 impairs breast cancer cell phenotypes by targeting and suppressing ubiquitin-conjugating enzyme E2T (UBE2T)

Area of Science:

• Oncology
• Molecular Biology
• Genetics

Background:

• Breast cancer presents a significant global health challenge with high morbidity.
• MicroRNAs (miRNAs) are increasingly recognized for their roles in cancer development.
• The specific function and regulatory mechanisms of miR-543 in breast cancer remain incompletely understood.

Purpose of the Study:

• To elucidate the molecular mechanisms underlying miR-543's involvement in breast cancer progression.
• To investigate the direct target of miR-543 and its downstream signaling pathways in breast cancer cells.
• To evaluate the therapeutic potential of miR-543 and its target gene in breast cancer treatment.

Main Methods:

• Quantitative real-time PCR (qRT-PCR) and Western blotting were used to assess mRNA and protein expression levels.
• Cell proliferation, viability, migration, and invasion were evaluated using CCK-8, BrdU, wound healing, and Transwell assays.
• Dual-luciferase reporter and RNA pull-down assays confirmed the direct interaction between miR-543 and UBE2T; in vivo tumor formation experiments were also conducted.

Main Results:

• miR-543 expression was significantly downregulated in breast cancer tissues and cell lines, while UBE2T expression was upregulated.
• miR-543 directly targets UBE2T, with a negative correlation observed between their expression levels in breast cancer tissues.
• Overexpression of miR-543 inhibited breast cancer cell viability, proliferation, migration, and invasion, and suppressed tumor growth in vivo by targeting UBE2T and inhibiting the ERK/MAPK pathway.

Conclusions:

• miR-543 acts as a tumor suppressor in breast cancer by directly targeting UBE2T.
• The miR-543/UBE2T axis regulates breast cancer progression via the ERK/MAPK signaling pathway.
• miR-543 and UBE2T represent promising therapeutic targets for clinical intervention in breast cancer.