Lnc00113 promotes triple-negative breast cancer progression via the NOB-1/MAPK signaling axis

Background

Triple-negative breast cancer (TNBC) represents the most aggressive form of breast cancer. While the involvement of long non-coding RNA (lncRNA) in the progression of TNBC has been demonstrated, the role of Lnc00113 in TNBC remains unexplored. We aimed to explore the function of Lnc00113 in TNBC.

Methods

Expression levels and the clinical significance of Lnc00113 were assessed in The Cancer Genome Atlas (TCGA) database. The expression levels of Lnc00113 in TNBC tissues and cell lines were examined using qRT-PCR (quantitative Real-Time Polymerase chain reaction). The proliferation, apoptosis and invasion abilities were evaluated using CCK-8 (Cell Counting Kit-8), EdU (5-Ethynyl-2'-deoxyuridine), apoptosis and transwell assays following Lnc00113 knockdown/overexpression. Dual-luciferase and fluorescence in situ hybridization assays were employed to detect the correlation between Lnc00113, miR-107 and Nin-one binding protein (NOB-1).

Results

We identified significant upregulation of Lnc00113 in TNBC tissues and cell lines, with high Lnc00113 expression correlating with advanced pathological staging and poorer prognosis in the TCGA database. Functional assessments through knockdown/overexpression experiments revealed that Lnc00113 promoted TNBC cell proliferation, apoptosis and invasion. Fluorescence in situ hybridization experiments showed cytoplasmic localization of both Lnc00113 and NOB-1. Dual-luciferase assays demonstrated direct binding between Lnc00113 and miR-107, while miR-107 directly interacted with NOB-1. Mechanistically, our findings indicated that Lnc00113 promotes TNBC progression through the miR-107/NOB-1/MAPK signaling axis.

Conclusion

Lnc00113 emerges as a potential driver of TNBC growth and progression through modulation of the NOB-1/MAPK signaling axis, providing insights into diagnostic biomarkers and therapeutic targets for TNBC.