Abstract. Breast cancer affects ~10% of women worldwide and is responsible for ~12% of all cancer-associated mortalities. Breast cancer is more prone to metastasis compared with other types of cancer. Up to 5% of patients with breast cancer present with incurable metastasis and an additional 10-15% of patients develop metastases within 3 years of their initial diagnosis. MicroRNAs (miRNAs) are short RNAs, 21-25 nucleotides in length, that have been shown to significantly affect gene expression. In total >2,000 miRNAs have been identified and specific miRNAs have been revealed to be associated with cancer. In the present study, we observed that the majority of breast cancer specimens collected expressed low levels of miR-202 compared with adjacent tissues and normal cell lines. Mechanistic investigations identified KRAS as a potential target gene of miR-202 and it was demonstrated that miR-202 exerted its tumor-suppressive effects by regulating the expression of KRAS in breast cancer cells. Functional assays revealed that miR-202 significantly reduced cell proliferation, migration and invasion in vitro. In summary, these results indicate the function of miR-202 in breast cancer progression and suggest that its use within breast cancer therapy is promising. IntroductionBreast cancer is one of the most common malignant tumors in women. In many areas, breast cancer is the most common malignancy in females. In China, the incidence of breast cancer is increasing annually. Because the development and progression of breast cancer are complex processes involving many genes, the underlying mechanism of breast cancer remains unclear (1,2).Single-stranded RNAs consisting of 19 to 25 nucleotides are known as microRNAs (miRNAs). These RNAs are regulatory molecules that modulate the expression of functional genes, play an important role in many biological processes, and are expressed in a tissue-and time-specific manner. miRNAs regulate gene expression at the post-transcriptional level mainly via completely complementary or partially complementary binding to the 3' UTR of the target gene, resulting in degradation or translational repression of the target gene (2-4). Studies have shown that a variety of miRNAs are involved in malignant transformation processes, such as malignant proliferation, metastasis and recurrence, and apoptosis inhibition. Studies have reported that miRNA inhibitors can reduce the high miR-21 expression in breast cancer cells, inhibiting proliferation and migration; that miR-373 can promote the metastasis of breast cancer cells; that miR-520 plays a role in promoting the development of breast cancer; and that miR-126 and miR-335 are able to inhibit breast cancer to a certain extent (5-7). Recent studies have demonstrated that miR-202 is associated with several types of cancer, miR-202 has a lower expression in several of cancers, and however, the expression and function of miR-202 have not been investigated in breast cancer (8).KRAS belongs to the RAS family; it is located on the short arm of chromosome 1...

MicroRNAs are a class of small noncoding RNAs that regulate the translation of target mRNA transcripts. MiR-592 has been considered to play important roles in the initiation and progression of cancer by targeting various molecules in several human cancers, but its role in glioma has not been explored. This study aims to explore the suppressive mechanism of miR-592 in the regulation of glioma development, an effect that is crucial for the further exploration of miR-592 as a novel therapeutic target for glioma. Our results proved that the expression of miR-592 was lower and the expression of Rho-associated protein kinase (ROCK1) was higher in glioma tissue than in adjacent tissue and that lower miR-592 expression was associated negatively with ROCK1 expression. Then, we showed that miR-592 was downregulated in glioma and could suppress the growth of the glioma cell lines U87 and U251. ROCK1, which is a known oncogene, was identified as a direct target of miR-592. A luciferase reporter assay indicated that miR-592 regulates ROCK1 expression through binding to its 3'-UTR. Furthermore, our results showed that miR-592 targets the ROCK1 transcript and suppresses glioma cell growth and invasive growth, thereby providing a potential therapeutic target for glioma treatment.

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