In conclusion, these results suggested that PLK4 may promote the carcinogenesis and metastasis of CRC, thus indicating that PLK4 may be considered a molecular target for CRC treatment.
Collectively, the results suggested that the ATAD2‑dependent transcriptional regulation of PLK4 promoted cell proliferation and tumorigenesis, as well as radioresistance in GBM, thus potentially inducing tumor recurrence.
Taken together, we demonstrate that miRNA-126/PLK-4 axis is critical for tumorigenesis and progression of HCC, and the newly identified PLK-4/ATR/CHEK1 pathway may be a potential therapeutic target for HCC treatment.
Polo like kinase-4 (PLK4) is one such kinase that appears in low abundance and plays a well-characterized role in centriole duplication.PLK4 deregulation (i.e. both overexpression and depletion of PLK4), leads to altered mitotic fidelity and thereby triggers tumorigenesis.