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This study was designed to detecting the influences of lncRNA MEG3 in prostate cancer. Aberrant lncRNAs expression profiles of prostate cancer were screened by microarray analysis. The qRT‐PCR and Western blot were employed to investigating the expression levels of lncRNA MEG3, miR‐9‐5p and QKI‐5. The luciferase reporter assay was utilized to testifying the interactions relationship among these molecules. Applying CCK‐8 assay, wound healing assay, transwell assay and flow cytometry in turn, the cell proliferation, migration and invasion abilities as well as apoptosis were measured respectively. LncRNA MEG3 was a down‐regulated lncRNA in prostate cancer tissues and cells and could inhibit the expression of miR‐9‐5p, whereas miR‐9‐5p down‐regulated QKI‐5 expression. Overexpressed MEG3 and QKI‐5 could decrease the abilities of proliferation, migration and invasion in prostate cancer cells effectively and increased the apoptosis rate. On the contrary, miR‐9‐5p mimics presented an opposite tendency in prostate cancer cells. Furthermore, MEG3 inhibited tumour growth and up‐regulated expression of QKI‐5 in vivo. LncRNA MEG3 was a down‐regulated lncRNA in prostate cancer and impacted the abilities of cell proliferation, migration and invasion, and cell apoptosis rate, this regulation relied on regulating miR‐9‐5p and its targeting gene QKI‐5.

Acute coronary syndrome caused by the rupture of atherosclerotic plaques is one of the primary causes of cerebrovascular and cardiovascular events. Neovascularization within the plaque is closely associated with its stability. Long non‐coding RNA (lncRNA) serves a crucial role in regulating vascular endothelial cells (VECs) proliferation and angiogenesis. In this study, we identified lncRNA HCG11, which is highly expressed in patients with vulnerable plaque compared with stable plaque. Then, functional experiments showed that HCG11 reversed high glucose‐induced vascular endothelial injury through increased cell proliferation and tube formation. Meanwhile, vascular‐related RNA‐binding protein QKI5 was greatly activated. Luciferase reporter assays and RNA‐binding protein immunoprecipitation (RIP) assays verified interaction between them. Interestingly, HCG11 can also positively regulated by QKI5. Bioinformatics analysis and luciferase reporter assays showed HCG11 can worked as a competing endogenous RNA by sponging miR‐26b‐5p, and QKI5 was speculated as the target of miR‐26b‐5p. Taken together, our findings revered that the feedback loop of lncRNA HCG11/miR‐26b‐5p/QKI‐5 played a vital role in the physiological function of HUVECs, and this also provide a potential target for therapeutic strategies of As.

Background RNA‐binding protein Quaking‐5 (QKI‐5), a major isoform of QKIs, inhibits tumor progression in non‐small cell lung cancer (NSCLC). However, the underlying molecular mechanisms of QKI‐5 in the cell cycle of NSCLC are still largely unknown. Methods MTT, flow cytometry, and colony formation assays were used to investigate cellular phenotypic changes. Mice xenograft model was used to evaluate the antitumor activities of QKI‐5. Co‐immunoprecipitation, RNA immunoprecipitation (RIP), and RIP sequencing were used to investigate protein–protein interaction and protein–mRNA interaction. Results The QKI‐5 expression was downregulated in NSCLC tissues compared with that in paired normal adjacent lung tissues. Overexpression of QKI‐5 inhibited NSCLC cell proliferative and colony forming ability. In addition, QKI‐5 induced cell cycle arrest at G0/G1 phase through upregulating p21Waf1/Cip1 (p21) expression and downregulating cyclin D1, cyclin‐dependent kinase 4 (CDK4), and CDK6 expressions. Further analyses showed that QKI‐5 interacts with p21 protein and CDK4, CDK6 mRNAs, suggesting a critical function of QKI‐5 in cell cycle regulation. In agreement with in vitro study, the mouse xenograft models validated tumor suppressive functions of QKI‐5 in vivo through altering cell cycle G1‐phase‐associated proteins. Moreover, we demonstrated that QKI‐5 is a direct target of miR‐31. The QKI‐5 expression was anticorrelated with the miR‐31 expression in NSCLC patient samples. Conclusion Our results suggest that the miR‐31/QKI‐5/p21‐CDK4–CDK6 axis might have critical functions in the progression of NSCLC, and targeting this axis could serve as a potential therapeutic strategy for NSCLC. miR‐31 mediated QKI‐5 downregulation promoted tumor growth of NSCLC through regulating p21 protein and CDK4/6 mRNAs.