<p>Aberrant Expression of miR-592 Is Associated with Prognosis and Progression of Renal Cell Carcinoma</p>

Abstract

PurposeMicroRNAs have recently reported playing a vital role in the development of cancers. However, the role of miR-592 in renal cell carcinoma (RCC) has not been explored. In this study, the potential role of miR-592 was investigated in RCC.Patients and methodsThe expression of miR-592 was evaluated in RCC tissues and cell lines using qRT-PCR assays. The Kaplan-Meier analysis and Cox proportional hazards model analysis was used to analyze the prognostic value of miR-592 in RCC. The effects of miR-592 on cell proliferation, migration, and invasion were determined by cell counting kit-8 (CCK-8) and Transwell assays in vitro.ResultsThe results showed that miR-592 was significantly increased both in RCC tissues and cell lines. Overexpression of miR-592 was significantly associated with lymph node metastasis, TNM stage, and poor overall survival. And functional studies in two RCC cell lines (786-O and Caki-1) have shown that overexpression of miR-592 promoted cell proliferation, migration, and invasion, while silence of miR-592 inhibited cell proliferation, migration, and invasion. SPRY2 was a direct target of miR-592.ConclusionOverall, overexpression of miR-592 may be a prognostic biomarker and therapeutic strategy for patients with RCC, which is correlated with the progression of RCC.

The Potential Role of Selected miRNA in Uveal Melanoma Primary Tumors as Early Biomarkers of Disease Progression

“…These results are contrary to several other studies showing that they usually act as tumor suppressors in pancreatic, colorectal, prostate, breast, and other cancers [21][22][23][24][25][26]. Similar to our studies, the overexpression of hsa-miR-592 was also described in progression of renal cell carcinoma, colorectal carcinoma with unaffected mismatch repair mechanisms, and gastric cancer [27][28][29]. In the case of hsa-miR-1247, its upregulation, contrary to our study, has shown its tumor suppressing properties in pancreatic carcinoma as well as in neuroblastoma [30,31].…”

Identification of MicroRNAs as Viable Aggressiveness Biomarkers for Prostate Cancer

“…When comparing the remaining potential miRNAs, according to the present bioinformatics analysis (miR-93-5p, miR-23c, miR-210-3p, miR-221-3p, and miR-592), all were suggested with important roles in PC screening [61], aggressiveness [8,62,63], and recurrence [7,18,64], or even new etiological values [65] were suggested. These miRNAs have also been highlighted with carcinogenic effects in other tumors, such as endometrial [66,67], osteosarcoma [68], hepatocellular [69], renal [17,70], or colorectal [71], among others [72][73][74]. According to our experimental analysis, miR-210-3p, miR-23c, and miR-592 were suggested as aggressiveness biomarkers in PC and miR-93-5p, miR-130b, and miR-141 were suggested as diagnostic biomarkers for this tumor.…”

“…As can be seen, there are many aspects that indicate miR-592 with interest for cancer aggressiveness biomarker and also for prognosis and therapeutics in patients with renal cell carcinoma. An over-expression of miR-592 is suggested to promote proliferation, migration, and invasion of renal cell carcinoma cells by targeting SPRY2 (gene related to PI3K/AKT and MAPK/EPK signaling pathways) [17]. In PC, there are also data relating miR-592 with aggressiveness in combination with ANPEP, miR-217, and miR-6715b [18].…”

Blood miRNAs miR-549a, miR-552, and miR-592 serve as potential disease-specific panels to diagnose colorectal cancer

“…Pan Z. et al have proposed that a high level of miR-592 serves as an indicator of a poorer prognosis in CRC patients [ 33 ]. However, it is worth noting that miR-592 expression has also been observed in other types of cancer, including renal cell carcinoma, prostate cancer, gastric cancer, and retinoblastoma cancer [ [35] , [36] , [37] ]. In 2017, Wang W. discussed the inhibitory effects of miR-592 on the proliferation, migration, and invasion of hepatocellular carcinoma through its targeting of IGF-1R [ 38 ].…”