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The long non‑coding RNA taurine up‑regulated gene 1 (TUG1) has been shown to be dysregulated in various types of malignant cancer; however, its underlying mechanism of action has not been fully elucidated. The present study aimed to investigate the biological role and clinical significance of TUG1 in the progression of colorectal cancer (CRC). A reverse transcription‑quantitative polymerase chain reaction assay was used to evaluate TUG1 expression in tissues from patients with CRC. The effect of TUG1 on cell viability of CRC cells using MTT assay. The influence of TUG1 on tumorigenesis was monitored using an in vivo xenograft model. The status of the Wnt/β‑catenin signaling pathway was evaluated using immunofluorescence, western blotting and luciferase reporter assays. The results demonstrated that the expression of TUG1 was positively associated with the pathological grade and clinical stage of CRC patients. Knockdown of TUG1 inhibited the proliferation of CRC cells and attenuated the activity of Wnt/β‑catenin pathway in CRC cells. In addition, TUG1 knockdown inhibited the tumorigenicity in the in vivo CRC xenograft model, as well as the nuclear localization of β‑catenin and downstream gene transcription. Taken together, the data of the present study highlighted the pivotal role of the TUG1‑Wnt/β‑catenin signaling pathway in CRC, which could be targeted to improve the therapeutic efficacy of CRC. [ABSTRACT FROM AUTHOR]

Epithelial membrane protein 3 (EMP3) is a transmembrane signaling molecule, which is important in the regulation of apoptosis, differentiation and invasion of cancer cells. However, the specific function and regulatory mechanism of EMP3 in primary breast carcinoma remain to be elucidated. In the present study, the mRNA and protein levels of EMP3 were observed to be upregulated in primary breast carcinoma tissues, compared with normal tissues. It was hypothesized that the overexpression of EMP3 was correlated with the downregulation of microRNA-765 (miR-765), an underexpressed miRNA in primary breast carcinoma tissues. Functional analysis demonstrated that EMP3 was regulated by miR-765 through binding to its 3'untranslated region. In addition, the knockdown of EMP3 and miR-765 had similar effects on the inhibition of proliferation and invasion in SK-BR-3 cells. These results provided novel insight into the regulatory mechanism of EMP3 in primary breast carcinoma. [ABSTRACT FROM AUTHOR]