Knockdown of lncRNA Enhances Radiosensitivity in Triple-Negative Breast Cancer Cells by Regulating / Axis.

BACKGROUND

Long non-coding RNAs (lncRNAs) have been reported to play essential roles in regulating the radiosensitivity of cancers. Prostate cancer-associated transcript 6 () exerts oncogenic roles in several tumors. However, the roles of and its underlying mechanism in regulating the radiosensitivity of triple-negative breast cancer (TNBC) have not been investigated.

METHODS

The expression levels of () and tumor protein D52 () were determined by quantitative real-time polymerase chain reaction (qRT-PCR). Cell viability, apoptosis and colony formation were assessed by Cell Counting Kit-8 (CCK-8) assay, flow cytometry and colony formation assay, respectively. The interaction between and or was predicted by bioinformatics analysis and verified by dual-luciferase reporter assay. Western blot was carried out to detect the protein level of TPD52.

RESULTS

and were highly expressed and was lowly expressed in TNBC tissues and cells, which was associated with an aggressive tumor phenotype in patients, affecting lymph node metastasis and clinical stage. or knockdown or overexpression enhanced the radiosensitivity of TNBC cells via inhibiting proliferation and inducing apoptosis. directly interacted with and negatively regulated expression. Moreover, was confirmed as a target of . Besides, regulated the radiosensitivity of TNBC cells through acting as a molecular sponge of to modulate expression.

CONCLUSION

Knockdown of promoted the radiosensitivity of TNBC cells through regulating / axis, providing a vital theoretical basis to improve the radiotherapy efficiency of TNBC.