Long non-coding RNA AC245100.4 promotes prostate cancer tumorigenesis via the microRNA-145-5p/RBBP5 axis

Long non-coding 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 miR-145-5p. This was further verified using a dual luciferase and RNA immunoprecipitation assays. AC245100.4 could positively regulate RBBP5 expression, but negatively regulated miR-145-5p expression. In addition, AC245100.4 knockdown-mediated inhibitory effects on cell proliferation and migration could be reversed by miR-145-5p silencing. Overall, the present study proposed a novel model in which the AC245100.4/miR-145-5p/RBBP5 ceRNA network induced the development of PCa, providing novel insights for PCa treatment.

Automated summary

The study found that AC245100.4 expression was significantly upregulated in prostate cancer and its knockdown inhibited tumor growth. Functional analysis showed that AC245100.4 played a role in regulating cell proliferation and migration, while mechanistic studies revealed its interaction with miR-145-5p and RBBP5 through a ceRNA network.