LINC00893 inhibits the progression of prostate cancer through miR-3173-5p/SOCS3/JAK2/STAT3 pathway

Abstract

Background Prostate cancer (PCa) is one of the most common malignant tumors in the male urinary system. In recent years, the morbidity and mortality of PCa have been increasing due to the limited effects of existing treatment strategies. Long non-coding RNA (lncRNA) LINC00893 was reported to inhibit the proliferation and metastasis of papillary thyroid cancer cells, but its role in PCa has not been reported. This study aims to investigate the role and underlying mechanism of LINC00893 in regulating the progression of PCa cells. Methods We first compared LINC00893 expression levels between PCa tissues and normal prostate tissues through TCGA database. The relative LINC00893 expression levels were further validated in 66 pairs of PCa tissues and para-cancerous normal tissues, as well as in PCa cell lines. Gain-of-function experiment was performed by transfecting PCa cell with LINC00893 expression vector, and CCK (Cell count kit)-8, 5-Ethynyl-2′-deoxyuridine (EdU) incorporation, colony information and transwell assays were conducted to assess the functional phenotypes. Dual-luciferase reporter, RNA-binding protein immunoprecipitation (RIP) and RNA pull-down assays were performed to evaluate the molecular interactions. Results LINC00893 was downregulated in PCa tissues and cell lines, and patients with low expression of LINC00893 were associated with a poorer overall survival rate. LINC00893 overexpression hindered the proliferation, epithelial-mesenchymal transition (EMT) as well as the migratory ability of PCa cells, and suppressed the tumorigenesis of PCa cells in nude mice. We further demonstrated that LINC00893 acted as a sponge for miR-3173-5p and inhibited its activity, which in turn regulated the suppressor of cytokine signaling 3 (SOCS3)/Janus Kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling axis. Conclusions Our study demonstrated that LINC00893 suppresses the progression of PCa cells through targeting miR-3173-5p/SOCS3/JAK2/STAT3 axis. Our data uncovers a novel tumor-suppressor role of LINC00893 in PCa, which may serve as a potential strategy for targeted therapy in PCa. Grapical Abstract

Identification of potential biomarkers and pathways for asthenozoospermia by bioinformatics analysis and experiments

“…For instance, LINC00893 o overexpression suppresses the proliferation, migration, or invasion of gastric cancer cells and regulates epithelial-mesenchymal transition by binding with RBFOX2 ( 35 ). LINC00893 inhibits the progression of prostate cancer through the miR-3173–5p/ SOCS3 / JAK2 / STAT3 pathway ( 36 ). LINC00893 overexpression abrogates the proliferation and migration abilities of papillary thyroid cancer cells via the PTEN/AKT pathway ( 37 ).…”

Identification of immune-related lncRNA in sepsis by construction of ceRNA network and integrating bioinformatic analysis

“…Previous research has shown that the expression of lncRNA LINC00265 was up-regulated in osteoarthritis patients and directly suppressed the expression of miR-101-3p; conversely, LINC00265 knockdown alleviated cell apoptosis and inflammation induced by caspase-3 in osteoarthritis [ 48 ]. Additionally, lncRNA LINC00893 regulated the suppressor of SOCS3/JAK2/STAT3 pathway by acting as a ceRNA to bind with miR-3173-5p in patient with prostate cancer [ 49 ]. The activation of JAK/STAT signaling pathways has diverse functions in the pathogenesis of sepsis [ 50 ].…”

Exploring the regulatory role of Linc00893 in asthenozoospermia: Insights into sperm motility and SSC viability

“…numerous studies have indicated that the self-renewal and proliferation of SScs are regulated by various factors, including lncrnas (19,20). recent research has revealed that the expression of linc00893 is inversely correlated with cell proliferation in various types of cancer and that it serves a pivotal role in inhibiting tumor progression (21)(22)(23)(24). However, the relationship between linc00893 and SScs remains unclear.…”