miR‑873 inhibits colorectal cancer cell proliferation by targeting TRAF5 and TAB1.

MicroRNA-873 (miR‑873) has been reported to be dysregulated in a variety of malignancies, however, the biological function and underlying molecular mechanism of miR‑873 in colorectal cancer (CRC) remain unclear. In the present study we found that the expression levels of miR‑873 were markedly decreased in CRC cell lines and tissues from patients. Statistical analysis revealed that miR‑873 expression was inversely correlated with the disease stage of CRC. Kaplan‑Meier survival analysis revealed that patients with CRC with lower miR‑873 expression had shorter overall survival rates. Additionally, downregulation of miR‑873 enhanced the proliferation of CRC cells, while upregulation of miR‑873 reduced this proliferation. Furthermore, we found that tumor necrosis factor (TNF) receptor-associated factor 5 (TRAF5) and TGF‑β activated kinase 1 (MAP3K7) binding protein 1 (TAB1) were direct targets of miR‑873 in CRC cells. A luciferase assay revealed that ectopic expression of miR‑873 significantly reduced nuclear factor κB (NF‑κB) luciferase activity, while ectopic expression of miR‑873 inhibitor enhanced luciferase activity, suggesting that downregulation of miR‑873 can activate NF‑κB signaling. Therefore, our findings established a tumor-suppressive role for miR‑873 in the inhibition of CRC progression, which may be employed as a novel prognostic marker and as an effective therapeutic target for CRC.

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