4.5 Article

The hsa-miR-3613-5p, a potential oncogene correlated with diagnostic and prognostic merits in kidney renal clear cell carcinoma

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PATHOLOGY RESEARCH AND PRACTICE
卷 251, 期 -, 页码 -

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ELSEVIER GMBH
DOI: 10.1016/j.prp.2023.154903

关键词

MicroRNA-3613; Kidney renal clear cell carcinoma; Diagnosis; Prognosis; Therapy

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This study reveals that the expression of hsa-miR-3613-5p is associated with Kidney renal clear cell carcinoma (KIRC). The overexpression of hsa-miR-3613-5p in KIRC tissues has diagnostic merit and is significantly correlated with poor overall survival of patients. Abnormal expression of hsa-miR-3613-5p is correlated with various clinical parameters in patients with KIRC. Furthermore, a regulatory network of hsa-miR-3613-5p in KIRC is identified and pathway enrichment analysis shows its involvement in cell cycle, cell adhesion molecules, and hepatocellular carcinoma pathways. These findings suggest that hsa-miR-3613-5p may serve as a valuable indicator for early detection, risk stratification, and targeted treatment of KIRC.
MicroRNA-3613 (hsa-miR-3613-5p), a biomarker with a dual role as an oncogenic or tumor suppressor, is associated with different types of cancer. This study aimed to determine the correlation between the hsa-miR3613-5p gene expression and Kidney renal clear cell carcinoma (KIRC). Utilizing several bioinformatics tools, we examined the expression level and clinicopathological value of hsa-miR-3613-5p in patients with KIRC compared to normal tissues. Other bioinformatic measures, including survival analysis, diagnostic merit of hsamiR-3613-5p, downstream target prediction, potential upstream lncRNAs, network construction, and functional enrichment analysis of hsa-miR-3613-5p, were performed. We observed that overexpression of hsa-miR-3613-5p in KIRC tissues had valuable diagnostic merit and was significantly correlated with the poor overall survival of KIRC patients. We also realized a correlation between abnormal expression of hsa-miR-3613-5p and several clinical parameters such as pathological stage, race, age, and histological grades in patients with KIRC. Moreover, we constructed the most potential regulatory network of hsa-miR-3613-5p in KIRC with 17 different axes, including four pseudogenes, two lncRNAs, and three mRNAs. Besides, we uncovered six variants in the mature form of hsa-miR-3613-5p. Finally, pathway enrichment analysis demonstrated that the top-ranked pathways for hsa-miR-3613-5p are cell cycle, cell adhesion molecules (CAMs), and hepatocellular carcinoma pathways. The present report suggests that the higher expression of hsa-miR-3613-5p is associated with the progression of KIRC. Therefore, it may be considered a valuable indicator for the early detection, risk stratification, and targeted treatment of patients with KIRC.

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