ArticleTranslational andrology and urology2026
miR-1251-5p inhibits tumorigenesis and metastasis in renal cell carcinoma by targeting MTHFD2.
Article in Translational andrology and urology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Renal cell carcinoma (RCC) is one of the most severe diseases worldwide. More and more studies have found that microRNAs (miRNAs) play very important roles in the occurrence and development of cancer. Previous studies showed that miR-1251-5p is lowly expressed in RCC. However, how miR-1251-5p is involved in regulating the growth and invasion of RCC cells is still unclear. This study aimed to determine the specific effect and molecular mechanism of miR-1251-5p in renal cancer. Our research may provide a new idea for the diagnosis and treatment of RCC. Methods: Bioinformatics analyses were performed using starBase, UALCAN, and ONCOLNC databases to evaluate the expression of miR-1251-5p in The Cancer Genome Atlas-Kidney Renal Clear Cell Carcinoma (TCGA-KIRC) dataset and its correlation with clinical characteristics of RCC. Cell Counting Kit-8 (CCK-8), colony formation, wound healing, and Transwell assays were utilized to assess the effects of miR-1251-5p on the proliferation and migration of RCC cells. Dual-luciferase reporter assay, quantitative real-time polymerase chain reaction (qRT-PCR), and Western blotting (WB) analysis were employed to identify and validate the downstream target gene of miR-1251-5p, and functional rescue experiments were conducted to confirm the regulatory relationship between miR-1251-5p and its target gene. Results: miR-1251-5p was significantly downregulated in TCGA-KIRC, patient blood samples, and RCC cell lines. Moreover, low miR-1251-5p expression was associated with advanced tumor grade, lymph node metastasis, and worse overall survival in RCC patients. Overexpression of miR-1251-5p effectively inhibited the proliferation and migration of RCC cells. Methylenetetrahydrofolate dehydrogenase 2 (MTHFD2) was identified as a direct downstream target of miR-1251-5p. MTHFD2 was highly expressed in RCC and correlated with poor prognosis. Knockdown of MTHFD2 suppressed RCC cell functions and reversed the tumor-suppressive effect induced by overexpression of miR-1251-5p. Conclusions: In the study, miR-1251-5p/MTHFD2 axis is shown to play a vital role in RCC. Therefore, targeting this axis may be a potential therapeutic target combating the progression of RCC.
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