RESUMO
Subsequently to the publication of the above article, an interested reader drew to the authors' attention that, concerning the cell proliferation and migration assay data shown in Figs. 6D and 7B, there were a pair of panels showing overlapping data, such that the same data had apparently been selected to show the results from different experiments. Subsequently, the authors referred back to their original data, and identified further incorrectly assembled data panels in Figs. 3B and 7B. The corrected versions of Fig. 3B (showing the correct data for the 'AC245100.4 / PC3 / 0 h' scratchwound assay data panel), Fig. 6D (showing the correct data for the 'PC3 / NCmimic' and 'DU145 / NCinhibitor' data panels) and Fig. 7D (showing the correct data for the 'PC3 / 24 h / InhibitormiR1455p + siAC245100.4' data panel) are shown on the subsequent pages. The authors regret the errors that were made during the preparation of the published figures, and confirm that these errors did not grossly affect the conclusions reported in the study. The authors are grateful to the Editor of Oncology Reports for allowing them the opportunity to publish a Corrigendum, and all the authors agree to this Corrigendum. Furthermore, they apologize to the readership for any inconvenience caused. [Oncology Reports 45: 619629, 2021; DOI: 10.3892/or.2020.7894].
RESUMO
Long noncoding RNAs (lncRNAs) are markedly involved in cancer progression. Thus, identification of these lncRNAs can aid in the treatment of cancer. The present study focused on investigating the overall biological function, mechanism of action and clinical importance of lncRNA AC245100.4 in prostate cancer (PCa). The present study identified that AC245100.4 expression was significantly upregulated in PCa tissues and cell lines. Knockdown of AC245100.4 impaired tumor growth in an animal model. Biological function analysis indicated that AC245100.4 overexpression notably promoted cell proliferation and migration, while knockdown of AC245100.4 suppressed cell proliferation and migration. Mechanism studies focused on the competing endogenous RNA (ceRNA) network of AC245100.4. Bioinformatics predictions indicated that both AC245100.4 and retinoblastoma binding protein 5 (RBBP5) had microRNA (miR) response elements for miR1455p. This was further verified using a dual luciferase and RNA immunoprecipitation assays. AC245100.4 could positively regulate RBBP5 expression, but negatively regulated miR1455p expression. In addition, AC245100.4 knockdownmediated inhibitory effects on cell proliferation and migration could be reversed by miR1455p silencing. Overall, the present study proposed a novel model in which the AC245100.4/miR1455p/RBBP5 ceRNA network induced the development of PCa, providing novel insights for PCa treatment.