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.
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.
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.