FOXC1-induced LINC01123 acts as a mediator in triple negative breast cancer

Area of Science:

• Oncology
• Molecular Biology
• Gene Regulation

Background:

• MicroRNAs (miRNAs) are non-coding RNAs with crucial roles in cellular processes.
• The specific functions of miRNAs in triple-negative breast cancer (TNBC) remain incompletely understood.
• This study investigates the role of microRNA-663a (miR-663a) in TNBC.

Purpose of the Study:

• To dissect the role of miR-663a in TNBC cellular processes.
• To identify regulatory mechanisms and downstream targets of miR-663a in TNBC.
• To explore the potential of miR-663a as a therapeutic target in TNBC.

Main Methods:

• Quantitative reverse transcription PCR (qRT-PCR) to assess miR-663a expression.
• Cell proliferation and apoptosis assays to evaluate miR-663a function.
• Bioinformatics, luciferase reporter assays, and ChIP to identify LINC01123 as a sponge for miR-663a and CMIP as its target, and FOXC1 as an inducer.

Main Results:

• miR-663a was significantly downregulated in TNBC cell lines compared to normal cells.
• Overexpression of miR-663a suppressed TNBC cell proliferation and induced apoptosis.
• LINC01123, a long non-coding RNA, acts as a sponge for miR-663a, inhibiting its function and protecting CMIP.
• FOXC1 transcriptionally activates LINC01123, forming a regulatory axis.

Conclusions:

• FOXC1 induces LINC01123, which then sponges miR-663a, leading to CMIP upregulation and promoting TNBC progression.
• This FOXC1-LINC01123-miR-663a-CMIP pathway represents a novel mechanism in TNBC development.
• Targeting this pathway may offer a new therapeutic strategy for TNBC.