The long non-protein coding RNA PCCA-DT exerts an oncogenic activity in non-small cell lung cancer by acting as a competing endogenous RNA to regulate the cell cycle through targeting the microRNA-20a-5p/CCND1 axis

Background: The long non-coding RNA PCCA-DT has yet to be thoroughly investigated, and its involvement in cancer remains largely unexplored. Yet, the detailed roles of PCCA-DT in non-small cell lung cancer (NSCLC) are currently mostly undefined. Herein, we examined the expression of PCCA-DT in NSCLC to clarify its clinic significance. We also explored the detailed functions of PCCA-DT in regulating the aggressive phenotype of NSCLC. Moreover, the precise mechanisms by which PCCA-DT exerts its carcinogenic actions in NSCLC were unraveled. Methods: We applied the data acquired from tissue specimens and TCGA database to analyse PCCA-DT level in NSCLC. Functional assays were implemented to address the regulatory effect of PCCA-DT in NSCLC. The mechanistic interaction among PCCA-DT, microRNA-20a-5p (miR-20a-5p), and cyclin D1(CCND1) was tested utilizing bioinformatics prediction, luciferase reporter assay and RNA immunoprecipitation. Results: A noticeable overexpression of PCCA-DT was affirmed by data from TCGA and our own cohort. Functionally, the absence of PCCA-DT produced tumor-repressing actions in NSCLC, and was taken part in the control of cell proliferation, colony-forming, edu and cell cycle. Mechanistically, as a competitive endogenous RNA, PCCA-DT decoyed miR-20a-5p and consequently overexpressed CCND1 in NSCLC cells. Ultimately, we conducted a sequence of recusing experiments, which highlighted that the regulatory activities of PCCA-DT deficient in repressing the malignant properties of NSCLC cells can be counteracted by hindering miR-20a-5p or overexpressing CCND1. Conclusion: PCCA-DT exerts as a crucial component to worsen the oncogenicity of NSCLC cells by targeting miR-20a-5p/CCND1 axis. Thus, the newly identified ceRNA pathway may have great potential as a diagnostic and prognostic biomarker, as well as an attractive therapeutic target for NSCLC.