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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, METHODS, RESULTS. Meshes: Adult, Animals, Apoptosis, Base Sequence, Binding Sites, CDC2-CDC28 Kinases, Carcinoma, Carcinoma, Papillary, Carrier Proteins, Case-Control Studies, Cell Cycle Proteins, Cell Line, Tumor, Cell Proliferation, Cell Transformation, Neoplastic, Disease Models, Animal, Female, Gene Expression, Gene Expression Regulation, Neoplastic, Humans, Male, Mice, MicroRNAs, RNA Interference, Signal Transduction, Spheroids, Cellular, Thyroid Cancer, Papillary, Thyroid Neoplasms, Tumor Burden, Tumor Cells, Cultured, Xenograft Model Antitumor Assays.
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Do miR-26a and its target CKS2 modulate cell growth and tumorigenesis of papillary thyroid carcinoma? Context: While many studies have shown that levels of miR-26a are lower in papillary thyroid carcinoma (PTC), the role and mechanism of miR-26a in PTC are unclear. We used database searches to select potential mRNA targets of miR-26a. Anti-miR-26a, miR-26a mimic, siRNA for CKS2 and their effects on cell growth, cell-cycle distribution and colony formation were evaluated. We also evaluate the over-expressed miR-26a in TPC-1 cells in severe combined immune-deficient mice. We used luciferase reporter assays, real-time PCR and western blot analysis to measure the expression and activity of miR-26a, CKS2, and related factors such as cyclin B1, cyclin A, cdk1, bcl-xl and Akt. Finally, we measured the relationship between the levels of miR-26a and CKS2 in PTC and normal thyroid tissues. Relative to normal thyroid tissues, miR-26a is consistently down-regulated in TPC specimens, and CKS2 was identified as a potential target. Up-regulated miR-26a expression or down-regulated CKS2 expression in TPC-1 and CGTH W3 cells lines caused G2 phase-arrest. Decreased miR-26a expression or increased CKS2 expression could have inverse function on PTC cell lines. CyclinB1, cyclinA, bcl-xl and AKt are indirectly regulated by miR-26a in a CKS2-dependent manner. Finally, CKS2 is overexpressed in PTC specimens relative to normal thyroid tissue, and a significant inverse correlation exists between miR-26a and CKS2 expression in clinical PTC specimens.
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Our data indicate that miR-26a functions as a growth-suppressive miRNA in PTC, and that its suppressive effects are mediated mainly by repressing CKS2 expression. Final Decision: yes