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The present study aimed to investigate the variations of the gene network and biological functions induced by hsa‑miR‑145‑5p in the laryngeal squamous cell carcinoma (LSCC) cell line Tu‑177. A hsa‑miR‑145‑5p‑overexpressed Tu‑177 cell model was established, and the gene expression microarray data of miR‑145‑5p‑overexpressed cells and negative control (NC) cells were analyzed. The differentially expressed genes (DEGs) between two groups were identified, and their potential functions were predicted by functional enrichment analysis. Furthermore, the targets of miR‑145‑5p were identified from the DEGs, and their potential functions and protein‑protein interactions (PPIs) were analyzed. The mRNA expressions of acetyl‑CoA carboxylase β (ACACB), fibroblast growth factor receptor 1 (FGFR1), protein phosphatase 3 catalytic subunit a (PPP3CA) and spleen associated tyrosine kinase (SYK), were analyzed via quantitative polymerase chain reaction. A total of 1,501 upregulated and 887 downregulated genes were identified in the hsa‑miR‑145‑5p‑overexpressed Tu‑177 cells, compared with the NC cells. Of these DEGs, 164 upregulated and 221 downregulated genes were predicted to be targeted by hsa‑miR‑145‑5p. The upregulated target genes were primarily associated with functions of immunity, whereas the downregulated target genes were significantly enriched in the p53 signaling pathway. In the PPI network consisting of 267 target genes, the upregulated ACACB had the greatest degree and interacted with downregulated genes including PPP3CA and SYK, in addition to upregulated genes, including FGFR1. The mRNA expressions of ACACB and FGFR1were markedly enhanced in miR‑145‑5p‑overexpressed Tu‑177 cells, whereas overexpressing miR‑145‑5p significantly reduced mRNA expression of PPP3CA and SYK. hsa‑miR‑145‑5p may exhibit an anticancer role in LSCC via regulating multiple cell processes, including cell proliferation and invasion, fatty acid metabolism, immunity and p53 signaling pathway. These findings provide novel information for the future investigation of miR‑145‑5p functions in LSCC. [ABSTRACT FROM AUTHOR]

Long non-coding RNAs (lncRNAs) have emerged recently as important factors in regulating fundamental biological processes. Alterations in the expression and function of lncRNAs have been observed to promote tumor formation, progression and metastasis. Although downregulation of the expression levels of LET lncRNA in several tumors has been reported, its role in gastric cancer remains unknown. The aim of the present study was to investigate the expression and function of LET in gastric cancer development. The expression levels of LET in 37 pairs of gastric cancer and adjacent non-tumor tissues were detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). In addition, LET expression in gastric cancer cell lines was analyzed by RT-qPCR assay analysis. Furthermore, the impact of LET on cell proliferation, migration and apoptosis were detected using the cell counting kit-8, wound scratch and ELISA assays, respectively. The results demonstrated that the expression level of LET was downregulated in gastric cancer tissues and cell lines (SGC-7901 and MGC-803) compared with normal tissues and a normal human gastric epithelial cell line (GES-1). Restoration of LET expression using a synthesized recombinant overexpression vector transfected into SGC-7901 and MGC-803 cells, significantly inhibited cell proliferation and migration, and promoted cell apoptosis in vitro. The present study is the first to demonstrate that LET may function as a tumor suppressor in gastric cancer. The results indicate that LET may be a promising biomarker and/or a therapeutic target for gastric cancer. [ABSTRACT FROM AUTHOR]

Rhomboid domain containing 1 (RHBDD1), is a member of the rhomboid protease family, which has a pivotal role in the progression of numerous severe malignancies. However, its role in colorectal carcinoma (CRC) remains to be elucidated. In the present study, RHBDD1 was shown to be widely expressed in CRC cell lines. Lentivirus-mediated RNA interference was employed to knockdown RHBDD1 expression in RKO CRC cells. Functional analyses indicated that depletion of RHBDD1 expression resulted in significantly reduced CRC cell proliferation and colony formation, and induced a G0/G1 phase cell cycle arrest. The findings of the present study suggest that RHBDD1 may contribute to CRC tumorigenesis and serve as a potential therapeutic target in human CRC. [ABSTRACT FROM AUTHOR]