Papillary thyroid cancer (PTC) is one of the most common cancers worldwide, and its carcinogenesis is influenced by a complex network of gene interactions. In this study, the microarray expression profile was re‐annotated into a lncRNA‐mRNA biphasic profile. LncRNA‐mRNA interactions were confirmed by established miRNA‐RNA data and hypergeometric test. Then, a PTC‐related lncRNA‐miRNA‐mRNA network (PTCRN) was constructed by integrating differentially expressed genes with the RNA‐RNA networks. The new network consisted of 21 lncRNAs, 241 mRNAs and 803 edges. To prioritize PTC‐related genes, we performed topological analysis and random walk with restart (PWR) algorithm analysis of PTCRN. Both analyses identified lncRNA RP11‐159F24.1 as a hub node in the network, which could interact with 47 mRNAs by sponging miR‐485. In functional enrichment analysis, these interacting mRNAs were associated with the pathways in cancer. In validation, RP11‐159F24.1 (up‐regulated; P = 0.0013) showed an opposite expression pattern with its target miR‐485 (down‐regulated; P = 0.0013) in PTC, indicating that the RP11‐159F24.1/miR‐485/mRNAs axis might play an important role in the development of PTC. In conclusion, this study has constructed a PTC‐related lncRNA‐miRNA‐mRNA network and identified the hub lncRNA RP11‐159F24.1 in the tumorigenesis, which provided novel insights to explore the underlying mechanism of PTC.

Previous investigations have proved that microRNA (miR)‐765 is significantly overexpressed in multiple tumor types. Nevertheless, the underlying molecular mechanism of miR‐765 in mediating breast carcinoma cell growth and metastasis remains unclear. Quantitative real‐time polymerase chain reaction was used to determine the levels of miR‐765 and inhibitor of growth 4 (ING4) in breast carcinoma tissues and breast carcinoma cells. Cell proliferation, colony formation, wound healing, and Transwell invasion assays were used to analysis the role of miR‐765 on breast carcinoma cell growth and aggressiveness. The expressions of ING4 were determined using Western blot analysis and immunohistochemical staining. The direct target of ING4 and miR‐765 was confirmed using the luciferase reporter assay. Nude mice were subcutaneously implanted with miR‐765 inhibitor transfected MDA‐MB‐231 cells to determine the potential role of miR‐765 in tumor growth in vivo. We observed that miR‐765 is overexpressed in breast carcinoma tissue and breast cancer cells. By using luciferase reporter gene bioassay, we find that ING4 is the direct target of miR‐765 in breast carcinoma. The level of ING4 is inversely associated with the level of miR‐765. The gain‐of‐function and loss‐of‐function experiments in vitro indicate that the downregulation of miR‐765 suppresses the growth, mobility, and invasion abilities of breast cancer cells by inhibiting ING4. In addition, overexpression of ING4 suppresses the aggressiveness of the MDA‐BA‐231 cell that is induced by miR‐761 in vitro. In this study, we prove that miR‐765 regulates the growth and metastasis of breast cancer via modulating miR‐765‐ING4‐negative feedback loop.

Gastric cancer (GC) remains a threat to the health of the global population. The present study investigated the effects and mechanisms of the long non-coding RNA myocardial infarction associated transcript (MIAT) on the proliferation, apoptosis and metastasis of GC (HGC-27 and AGS) cells. The expression levels of MIAT, micoRNA (miR)-331-3p and RAB5B mRNA were analyzed using reverse transcription-quantitative PCR analysis. Cell growth, apoptosis, migration and invasion were measured using 5-ethynyl-2′-deoxyuridine, flow cytometry, wound healing and Transwell assays, respectively. A luciferase assay was used to determine whether miR-331-3p targeted MIAT and RAB5B. The results indicated that MIAT levels were significantly upregulated in GC tissues and cells, correlated with RAB5B levels and inversely associated with miR-331-3p levels. MIAT overexpression promoted proliferation and metastasis, and inhibited the apoptosis of GC cells . MIAT knockdown had the opposite effect on GC cells . The rescue experiments revealed that the effects of MIAT knockdown on the biological behaviour of GC cells were attenuated by RAB5B overexpression. These data suggest that MIAT promotes GC progression via modulating miR-331-3p/RAB5B pathway.