Background: Long non-coding RNAs (lncRNAs) have been reported to play essential roles in regulating the radiosensitivity of cancers. Prostate cancer-associated transcript 6 (PCAT6 ) exerts oncogenic roles in several tumors. However, the roles of PCAT6  and its underlying mechanism in regulating the radiosensitivity of triple-negative breast cancer (TNBC) have not been investigated.
Methods: The expression levels of PCAT6, microRNA-185-5p  (miR-185-5p ) and tumor protein D52 (TPD52 ) 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 miR-185-5p  and PCAT6  or TPD52  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: PCAT6  and TPD52  were highly expressed and miR-185-5p  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. PCAT6  or TPD52  knockdown or miR-185-5p  overexpression enhanced the radiosensitivity of TNBC cells via inhibiting proliferation and inducing apoptosis. PCAT6  directly interacted with miR-185-5p  and negatively regulated miR-185-5p  expression. Moreover, TPD52  was confirmed as a target of miR-185-5p . Besides, PCAT6  regulated the radiosensitivity of TNBC cells through acting as a molecular sponge of miR-185-5p  to modulate TPD52  expression.
Conclusion: Knockdown of PCAT6  promoted the radiosensitivity of TNBC cells through regulating miR-185-5p /TPD52  axis, providing a vital theoretical basis to improve the radiotherapy efficiency of TNBC.
Keywords: triple-negative breast cancer, PCAT6 , miR-185-5p , TPD52 , radiosensitivity