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MicroRNAs (miRNAs) are a class of non-coding RNAs, containing about 22 nucleotides and having a pivotal function in various cellular processes. The oncogenic and tumor suppressor roles of miRNAs have been identified in cancers especially in gastric cancer, which is one of the most prevalent cancers. MiR-299-5p is located in the imprinted Dlk1-Dio3 region in chromosome 14q32. Aberrant expression of miR-299-5p was determined in solid and blood cancers. The current study was performed to assess the expression pattern of miR-299-5p in intestinal-type gastric adenocarcinoma and compare it with the normal adjacent counterparts. The expression level of miR-299-5p was investigated in forty fresh specimens which were obtained from gastric cancer patients during endoscopy. Moreover, the association of aberrant expression of miR-299-5p and clinicopathological features, as well as the susceptibility of miR-299-5p as a tumor marker, was determined. The result of qRT-PCR revealed the downregulation of miR-299-5p in intestinal-type gastric adenocarcinoma compared with adjacent tumor-free tissues (P < 0.001); this misregulation can be used as a tumor marker. Analysis of miR-299-5p misregulation did not reveal a significant correlation with clinical features. The result obtained from the present study revealed the significant downregulation of miR-299-5p in intestinal-type gastric adenocarcinoma which is consistent with previous studies showing miR-299-5p downregulation in other types of cancers. The data obtained from the current study suggest basic information which can be very helpful for future research in the field of diagnosis and treatment of gastric cancer.

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MicroRNAs (miRNAs) are impressive regulators of gene expression that have a critical role in the pathogenesis of colorectal cancer (CRC). With respect to the aberrant expression of miRNA-383 (miR-383) in some types of human malignancy, this prospective study characterized its contribution to CRC tumorigenesis. The real-time reverse transcriptionpolymerase chain reaction was used to examine miR-383 expression levels prospectively in 40 sample pairs of CRC tissues and adjacent noncancerous tissues (>2 cm from cancer tissue). No significant relationship was found between miR-383 expression levels and clinicopathological features. The ability of miR-383 to function as a tumor marker was also examined. Showing significant changes overall, miR-383 expression levels were significantly down regulated in the group of CRC samples compared with matched noncancerous tissue samples. A receiver-operating characteristic (ROC) curve also showed ROC area of 70% for miR-383 with 68 and 75% sensitivity and specificity, respectively. Therefore, miR-383 can be considered as a tumor marker in CRC and help as a potential predictive biomarker in the diagnosis of colorectal cancer.

With regard to recent increased rate of CRC in the world, the present study may be a contribution, though very small, in the diagnosis and consequently in the treatment of CRC patients.

Colorectal cancer (CRC) is one of the most common cancers in the world; therefore, extensive research is needed to find new molecular therapeutic targets and biomarkers. LncRNA (long non-coding RNA), a new class of non-coding RNAs, has a crucial role in the onset and progression of various cancers including colorectal cancer. Research on lncRNA is still at initial stages and underlying molecular mechanisms of the vast majority of lncRNA have remained unclear. LOC100287225 is one of these novel lncRNAs (long intergenic non-coding RNA) located in the long arm of the chromosome 18. The purpose of this study was to determine the expression of LOC100287225 in colorectal tissue, and its misregulation in CRC patients. Quantitative real-time-PCR (qRT-PCR) was used to investigate the LOC100287225 expression in pairs of tumorous and adjacent tumor-free tissues of 39 colorectal cancer patients. Also, the relationship between the clinicopathology and expression of LOC100287225 was determined. QRT-PCR results revealed that not only is LOC100287225 expressed in the intestinal tissue, but has also been misregulated during tumorigenesis. Moreover, LOC100287225 RNA relative expression levels were significantly lower in tumor tissues compared with adjacent tumor-free tissues (P< 0.001). RNA expression level of LOC100287225 did not show significant correlation with clinical characteristics. In conclusion, our study demonstrated that LOC100287225 misregulation could be a potential target for gene therapy in colorectal cancer.

Background: The Notch signaling pathway has a key role in angiogenesis and Delta-Like Ligand 4 (DLL4) is one of the main ligands of Notch involved in cell proliferation in sprouting vessels. Objective: In this study, we aimed to evaluate the expression of DLL4 in primary breast tumors and to examine the effect of melatonin on DLL4 expression in vitro. Methods: Eighty-five breast tumor and paired adjacent non-tumor tissue samples were collected. Apoptosis assay was performed on breast cancer cells to evaluate melatonin effects. Western blot and quantitative RT-PCR were used to measure DLL4 expression. Then, we investigated the effect of melatonin on the expression of DLL4 in four breast cancer cell lines at RNA and protein levels. We also performed Probabilistic Neural Network analysis to study genes closely associated with DLL4 expression. Results: Our results showed a significantly higher expression of DLL4 in tumor tissues as compared to non-tumor tissues (P = 0.027). Melatonin treatment substantially attenuated DLL4 expression in BT474 and MCF-7 cells, but not in SK-BR3 and MDA-MB-231 cells. Also, melatonin induced apoptosis in all four cell lines. Network analysis revealed a set of 15 genes that had close association and interaction with DLL4. DLL4 was overexpressed in breast cancer tissues as compared to the non-tumor tissues. Conclusion: It can be concluded that melatonin treatment attenuated DLL4 expression only in estrogen-responsive breast cancer cells and is able to induce apoptosis in breast cancer cells.