Malignant neoplasms are regarded as the main cause of death around the world; hence, many research studies were conducted to further perceive molecular mechanisms, treatment, and cancer prognosis. Cancer is known as a major factor for health‐related problems in the world. The main challenges associated with these diseases are prompt diagnosis, disease remission classification and treatment status forecast. Therefore, progressing in such areas by developing new and optimized methods with the help of minimally invasive biological markers such as circular microRNAs (miRNAs) can be considered important. miRNA interactions with target genes have specified their role in development, apoptosis, differentiation, and proliferation and also, confirm direct miRNA function in cancer. Different miRNAs expression levels in various types of malignant neoplasms have been observed to be associated with prognosis of various carcinomas. miR‐9 seems to implement opposite practices in different tissues or under various cancer incidences by influencing different genes. Aberrant miR‐9 levels have been observed in many cancer types. Therefore, we intended to investigate the precise role of miR‐9 in patients with malignant neoplasms. To this end, in this study, we attempted to examine different studies to clarify the overall role of miR‐9 as a prognostic marker in several human tumors. The presented data in this study can help us to find the novel therapeutic avenues for treatment of human cancers.

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Background: Identification of competing endogenous RNAs (ceRNAs), especially circRNAs, have become new hotspots in cancer researches. Although, their roles and underlying mechanisms in colorectal cancer (CRC) development remain mostly unknown. The aim of this study was to integrate both coding and non-coding available microarray data in development of CRC coupled with bioinformatics analyses to understand a more inclusive pathobiologic map regarding their molecular interactions and functions. Methods: The microarray data were retrieved from the Gene Expression Omnibus (GEO) database and analyzed. Several bioinformatics tools and databases including CircInteractome, CSCD, miRTarbBase, TargetScan, miRmap, GEPIA, STRING, Enrichr, DAVID, and MCODE were applied for further elucidation. Principal component analysis (PCA) has seperatly run for four datasets. The dysregulated circRNA-miRNA-mRNA network in CRC was constructed by Cytoscape. In addition, co-expression and protein-protein interaction (PPI) networks were established based on differentially expressed (DE) protein coding genes in CRC. Results: PCA disclose colorectal tumor and normal tissuses could be distinguished not only by mRNAs expression profile, but also by both circRNAs and miRNAs expression profiles. We identified 14 DE mRNAs (commonly between two datasets), 85 DE miRNAs and 36 DE circRNAs in CRC tissues compared with normal tissues. Taking their potential interactions into account, a circRNA-miRNA-mRNA network was constructed. Then, according to ceRNA hypothesis, the axes with expression in the desired direction were extracted. Our results disclosed some DE circRNAs with potential oncogenic (circ_0014879) or tumor suppressive (circ_0001666 and circ_0000977) effects. Finally, PPI network suggests pivotal roles for DOCK2 and PTPRC dysregulation in progression of CRC, possibly by facilitating of tumor escape from immune surveillance. Conclusion: Current study proposes a novel regulatory network consisting of DE circRNAs, miRNAs and mRNAs in CRC development that in turn highlights the roles of DE circRNAs at the upstream of oncotranscriptomic cascade in CRC development, suggesting their potentiality to be utilized as both prognostic and therapeutic biomarker.

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MicroRNA-135 (miR-135) is a microRNA which is involved in the pathoetiology of several neoplastic and non-neoplastic conditions. Both tumor suppressor and oncogenic roles have been reported for this miRNA. Studies in prostate, renal, gallbladder and nasopharyngeal cancers as well as glioma have shown down-regulation of miR-135 in cancerous tissues compared with controls. These studies have also shown the impact of miR-135 down-regulation on enhancement of cell proliferation and aggressive behavior. Meanwhile, miR-135 has been shown to be up-regulated in bladder, oral, colorectal and liver cancers. Studies in breast, gastric, lung and pancreatic cancers as well as head and neck squamous cell carcinoma have reported dual roles for miR-135. Dysregulation of miR-135 has also been noted in various non-neoplastic conditions such as Alzheimer’s disease, atherosclerosis, depression, diabetes, Parkinson, pulmonary arterial hypertension, nephrotic syndrome, endometriosis, epilepsy and allergic conditions. In the current review, we summarize the role of miR-135 in the carcinogenesis as well as development of other disorders.