The object of this study was to analyze the expression of miR-194 and miR-29 in gastric cancer and their roles in the regulation of malignant phenotype of gastric cancer cells, and to explore the application value of miR-194 and miR-29 in diagnosis and prognosis of gastric cancer. Tumor tissue and adjacent healthy tissue of 165 gastric cancer patients diagnosed by pathologic examinations were collected. Expression of miR-194 and miR-29 in the tissues was detected by RT-PCR. The relationship between miR-194 and miR-29 expression and clinical data was analyzed. SGC7901 cells were treated with miR-194 and miR-29 mimics, respectively. Effects of miR-194 and miR-29 on proliferation and invasion of SGC7901 cells were investigated. Expression levels of miR-194 and miR-29 in tumor tissue were lower than those in adjacent tissues (P<0.001). There was no significant difference in expression level of miR-194 and miR-29 in cancer tissues derived from gastric cancer patients in different age and gender groups (P>0.05). Expression of miR-194 and miR-29 in tumor tissue was closely related to TNM stage, differentiation degree of cancer cells and lymph node metastasis (P<0.05). Proliferation and migration of SGC7901 cells were significantly inhibited by miR-194 mimic and miR-29 mimic transfection (P<0.05). miR-194 and miR-29 are downregulated in gastric cancer, and the expression levels of miR-194 and miR-29 were closely related to tumor differentiation and metastasis. Overexpression of miR-194 and miR-29 significantly inhibited the proliferation and migration of gastric cancer. The detection of the expression of miR-194 and miR-29 can provide basis for the diagnosis and prognosis of gastric cancer.
Accumulated evidence has demonstrated that dysregulation of microRNAs (miRNAs) contributes to tumourigenesis and tumour development of glioblastoma multiforme (GBM). Therefore, miRNAs may be promising candidates in the development of prognosis biomarkers and effective therapeutic targets for patients with GBM. A number of studies have reported that miRNA‑574 (miR‑574) is aberrantly expressed in multiple types of human cancers. However, the expression pattern, biological functions and molecular mechanism of miR‑574 in GBM are yet to be elucidated. Therefore, the present study aimed to determine the expression level and biological functions of miR‑574 in GBM and the underlying molecular mechanisms. In the present study, miR‑574 levels were measured by reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) and were demonstrated to be significantly downregulated in human GBM tissues and cell lines. Functional experiments indicated that restored expression of miR‑574 using mimics led to the inhibition of the cell proliferation and invasion of GBM cells, as determined by Cell Counting kit‑8 and Matrigel invasion assays, respectively. In addition, bioinformatics analysis predicted that zinc finger E‑box‑binding homeobox 1 (ZEB1) may be a target of miR‑574. Subsequent RT‑qPCR, western blot analysis and luciferase reporter assays confirmed that ZEB1 was a direct target of miR‑574 in GBM. Additionally, ZEB1 was demonstrated to be upregulated and inversely correlated with miR‑574 expression in clinical GBM tissues. Rescue experiments demonstrated that overexpression of ZEB1 attenuated the inhibitory effects of miR‑574 on the proliferation and invasion of GBM cells. Overall, the results of the present study highlighted the potential tumour inhibitory roles of miR‑574 in GBM, thereby indicating that miR‑574 may be a novel and efficient therapeutic target for the treatment of patients with GBM.
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