Renal cell carcinoma (RCC) includes 2.2% of all diagnosed cancers and 1.8% of cancer-related mortalities. The available biomarkers or screening methods for RCC suffer from lack of sensitivity or high cost, necessitating identification of novel biomarkers that facilitate early diagnosis of this cancer especially in the susceptible individuals. MicroRNAs (miRNAs) have several advantageous properties that potentiate them as biomarkers for cancer detection. Expression profile of miRNAs has been assessed in biological samples from RCC patients. Circulatory or urinary levels of certain miRNAs have been proposed as markers for RCC diagnosis or follow-up. Moreover, expression profile of some miRNAs has been correlated with response to chemotherapy, immunotherapy or targeted therapeutic options such as sunitinib. In the current study, we summarize the results of studies that assessed the application of miRNAs as biomarkers, therapeutic targets or modulators of response to treatment modalities in RCC patients.

/pdf/microrna-signature-in-renal-cell-carcinoma-1y0f09vm55.pdf

MicroRNA Signature in Renal Cell Carcinoma.

Background Metastasis is the main cause of renal cell carcinoma (RCC) tumor death, and effective inhibition of RCC metastasis is an essential means to meliorate the prognosis of RCC patients. MicroRNAs (miRs) have been proved to be stable and important biomarkers for several malignancies. This study is therefore set out to explore the metastasis-related miR and its mechanism in RCC. Methods The expression of miR- 26a -5p in RCC was analyzed using the expression profile in the Cancer Genome Atlas (TCGA). MiR-26a-5p and E2F transcription factor 7 (E2F7) in RCC patients were detected by qRT-PCR. Cell Counting Kit-8 (CCK-8) was adopted to assess cell proliferation, Transwell was utilized to evaluate migration and invasion, and flow cytometry (FC) was used to determine apoptosis. Mouse cell-derived and patient-derived xenotransplantation models were established to evaluate the effect of miR-26a-5p on tumor growth and metastasis in vivo. The molecular mechanism of miR-26a-5p was analyzed by dual-luciferase reporter (DLR) gene analysis, qRT-PCR, and Western blot (WB) both in vivo and in vitro. Results MiR-26a-5p was reduced in renal carcinoma cells and may serve as a biomarker for renal cancer metastasis and prognosis. MiR-26a-5p up-regulation inhibited migration and invasion in renal cell lines and tumor metastasis in vivo. Bioinformatics target prediction and RNA-seq results showed that E2F7 was among the targets of miR-26a-5p and was significantly inhibited by miR-26a-5p in vivo and in vitro. Conclusion MiR-26a-5p presents low expression in RCC and promotes RCC cell apoptosis and prevents cells from proliferating and invading by targeting E2F7, which is a promising therapeutic target for RCC.

Up-Regulation of miR-26a-5p Inhibits E2F7 to Regulate the Progression of Renal Carcinoma Cells

Background Non-small cell lung carcinoma (NSCLC) is a malignancy with the highest mortality rate. Currently, surgery combined with radiotherapy is the first choice in the clinical treatment of lung carcinoma (LC); however, long-term radiotherapy leads to radiation resistance in patients, resulting in treatment failure. Methods In this study, a new microRNA-218-5p (miRNA-218-5p) was identified, and its function in LC was investigated. Results Reverse transcription quantitative polymerase chain reaction (RT-qPCR) results revealed that miRNA-218-5p was downregulated in LC. Overexpression or inhibition of miRNA-218-5p in LC and targeted binding of protein kinase, DNA-activated, catalytic polypeptide (PRKDC) to miRNA-218-5p were confirmed by comprehensive bioinformatic analysis. Exosomes from A549 and H1299 cells were cocultured with miRNA-218-5p and then cotransfected into radiation-resistant A549R and H1299R cells; the proliferation of radiation-resistant LC cells was found to be effectively inhibited and apoptosis was induced. Overexpression of miRNA-218-5p and X-irradiation could enhance the radiosensitivity of LC cells. Exogenous miRNA-218-5p derived from A549 and H1299 cells could be transfected into radiation-resistant LC cells and could inhibit PRKDC expression, thus accelerating DNA damage, apoptosis, and radiation sensitization of LC cells. Conclusions miRNA-218-5p could induce apoptosis and enhance the radiosensitivity of LC cells through regulatory activities, thus suggesting its application as a potential target for LC treatment.

https://onlinelibrary.wiley.com/doi/pdf/10.1111/1759-7714.13939

miRNA‐218‐5p increases cell sensitivity by inhibiting PRKDC activity in radiation‐resistant lung carcinoma cells

The dysregulation of circular RNAs (circRNAs) has been proved to be involved in the carcinogenesis of various cancers. Nevertheless, the biological function of circSLC7A6 remains unclear in Wilms' tumor (WT). In our study, we found that circSLC7A6 was upregulated in cancerous WT tissues and cells. Cell apoptosis was increased while cell viability, migration, and invasion were repressed by circSLC7A6 silencing. Besides, circSLC7A6 knockdown suppressed WT tumor growth in vivo. miR-107 was identified as a direct target of circSLC7A6, and circSLC7A6 could negatively regulate miR-107 expression. In addition, circSLC7A6 knockdown inhibited WT progression, while the effect was partially abolished by the downregulation of miR-107. Additionally, ABL proto-oncogene 2 axis (ABL2) was verified as a downstream gene of miR-107, and circSLC7A6 could upregulate ABL2 expression by serving as a ceRNA of miR-107. Moreover, functional assays revealed that ABL2 overexpression reversed the impact of circSLC7A6 depletion on cell proliferation, migration, invasion, and apoptosis of WT. In conclusion, the present study demonstrated that circSLC7A6 facilitated WT progression by upregulating ABL2 through inhibiting miR-107 expression. These results suggested that circSLC7A6 might serve as a potential therapeutic target for WT.

CircSLC7A6 promotes the progression of Wilms' tumor via microRNA-107/ ABL proto-oncogene 2 axis.

Renal cell carcinoma (RCC) is the most prevalent cancer of the kidney worldwide. Although the last decades showed advancement in diagnostic and therapeutic techniques for RCC, still patients diagnosed in the late stages of the disease showed a high percentage of recurrence and anticancer therapeutics resistance. In this sense, new biomarkers for RCC diagnosis/prognosis and targeted therapy are urgently required. In the last decade the highly advanced genome and transcriptome sequencing techniques have identified a family of noncoding RNAs (ncRNAs), including microRNAs, long noncoding RNAs, and circular RNAs, among others, as powerful regulators of numerous genes and pathways implicated in the development and progress of cancers, including RCC. Accumulating evidence indicated that dysregulated signatures of this family of ncRNAs could be applied as newly emerged diagnostic/prognostic genetic biomarkers and/or molecular targets for RCC therapeutic intervention. In this chapter the authors highlighted and discussed the main themes related to ncRNAs in RCC for their potential translational application in the clinic in the near future. 

Applications of noncoding RNAs in renal cancer patients

Although micro RNA (miRNA) expression profiles are widely investigated in renal cell carcinoma (RCC), their potential roles for affecting RCC initiation and progression remain largely unknown. Here, we examined the aberrant expression profiles of miRNAs inhuman metastatic RCC tissues based on Gene Expression Omnibus (GSE37989). We further validated them iRNAs expression data in the largest clinical dataset: The Cancer Genome Atlas (TCGA). And cell adhesion and migration abilities and epithelial me senchymal transition (EMT) related proteins were assessed in both normal and tumor RCC cell lines. We suggest that hsa-miR-143 is a potential tumor suppressor in RCC as its down regulation positively correlated with adverse prognosis. Biologically, cell adhesion, migration, and EMT were dramatically inhibited by miR-143. Mechanistically, we found that miR-143 targets ABL proto-oncogene 2 (ABL2), which was also found to be an indicator for poor survival in TCGA database. Our results have important implications in understanding functions of miRNAs in metastatic RCC and will provide a basis for further clinical application.

https://onlinelibrary.wiley.com/doi/pdf/10.1002/kjm2.12207

miR-143 inhibits renal cell carcinoma cells metastatic potential by suppressing ABL2.

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miR-143 inhibits renal cell carcinoma cells metastatic potential by suppressing ABL2.