LINC00106/RPS19BP1/p53 axis promotes the proliferation and migration of human prostate cancer cells

Abstract

Background Prostate cancer (PCa) is among the most prevalent cancers in males with high biochemical recurrence risk. LINC00106 contributes to the carcinogenesis of Hepatocellular carcinoma (HCC). However, it is unclear how it affects PCa advancement. Here, we studied LINC00106’s effects on PCa cells’ ability to proliferate, invade, and metastasize. Methods The data of LINC00106 from The Cancer Genome Atlas (TCGA) in human PCa tissues were analyzed using TANRIC and survival analysis. In order to determine the expression levels of genes and proteins, we also performed reverse transcription-quantitative PCR and western blot analysis. The migration, invasion, colony formation, and proliferation (CCK-8) of PCa cells with LINC00106 knockdown were investigated. The impact of LINC00106 on cell proliferation and invasion was also analyzed in mice. LncRNA prediction software catRAPID omics v2.1 (catRAPID omics v2.0 (tartaglialab.com)) was used to predict proteins that might interact with LINC00106. The interactions were verified via RNA immunoprecipitation and RNA pull-down assays and finally, the interaction between LINC00106 and its target protein and the p53 signaling pathway was studied using a dual-luciferase reporter assay. Results In PCa, LINC00106 was over-expressed in comparison to normal tissues, and it was linked to an unfavorableprognosis. In vitro and in vivo analyses showed that downregulating LINC00106 decreased PCa cells’ability to proliferate and migrate. A common regulatory axis generated by LINC00106 and RPS19BP1 prevents p53 activity. Conclusion Our experimental data indicate that LINC00106 functions as an oncogene in the onset of PCa, and the LINC00106/RPS19BP1/P53 axis canserve as a novel therapeutic target for PCa treatment.

Nanotherapeutic approaches for delivery of long non-coding RNAs: an updated review with emphasis on cancer

“…37 There was a co-regulatory relationship between LINC00106 and RPS19BP1 that inhibited p53 activity, promoting PCa cell proliferation and migration. 38 KRAS, TP53, CDKN2A, and SMAD4 are the four most frequently mutated genes associated with PaC, and they are considered to be the four major drivers of PaC. 39 As a ceRNA, lncRNA-UCA1 increased KRAS expression by sponging miR-590-3p and enhanced phospho-KRAS activity by increasing the binding of hnRNPA2B1 to KRAS via lncRNA-UCA1, which in turn increased UCA1 expression, enhancing the stemness and proliferation of PDAC cells.…”