Overexpression of microRNA miR-181a may have tumorigenic effects among patients with clear cell renal cell carcinoma (ccRCC) through inhibition of KLF6, according to a study published in Urologic Oncology.1
Previous studies have associated miR-181a dysregulation with various cancers, such as acute lymphoblastic leukemia as well as colon, breast, and pancreatic cancers, but its role in ccRCC is unknown.
For this study, researchers obtained tumor samples from 42 patients with ccRCC and used quantitative real-time polymerase chain reaction (qRT-PCR) assays to determine miR-181a expression.
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miR-181a was upregulated in ccRCC cells compared with normal tissues (P < .001), as well as in surrounding non-tumor tissues and in the 786-O, 769-P, A498, and CAKI-1 RCC cell lines (P < .001).
miR-181a levels were significantly associated with various aspects of tumor characteristics, including tumor size (P = .015), tumor necrosis (P = .023), Fuhrman grade (P = .002), and TNM staging (P < .001).
Not only was there a downregulation of KLF6 protein (P < .001) in ccRCC, but there were fewer KLF6-positive cells compared with normal tissues (P < 001). Researchers also discovered a negative correlation between miR-181a and KLF6 mRNA levels (r2 = .091, P < .01).
The study demonstrated that ccRCC cells overexpress miR-181a, which leads to acceleration of the cell cycle and apoptosis inhibition by KLF6 suppression. The authors concluded that these “results reveal a novel molecular role of miR-181a in ccRCC tumorigenesis and indicate that miR-181a may be a potential therapeutic target for ccRCC treatment.”
Reference
- Lei Z, Ma X, Li H, et al. Up-regulation of miR-181a in clear cell renal cell carcinoma is associated with lower KLF6 expression, enhanced cell proliferation, accelerated cell cycle transition, and diminished apoptosis. Urol Oncol. 2017 Oct 20. doi: 10.1016/j.urolonc.2017.09.019 [Epub ahead of print]
