Sequence-specific primers and fluorescence-labeled probes complementary to EI24, YWHAE, TFRC, CORO1C, S100A16, NLK, RAB1B, DEDD, CUL5, and PRDX3 and the endogenous reference GAPDH were used.
Six mRNAs were selected that exhibited an enrichment in the Ago complexes from PCa cells and were therefore potentially downregulated in cell lines and tumors: Etoposide induced 2.4 mRNA (EI24, alias p53-induced gene 8 protein), S100 calcium binding protein A16 (S100A16), Nemo-like kinase (NLK), RAS oncogene family member 1B (RAB1B), death effector domain-containing protein (DEDD), and cullin 5 (CUL5).
A reduction of CUL5 expression was found, for instance, in breast cancer , but so far not in prostate carcinoma.
For example, PPIA, TSG101, TRIM5[alpha], APOBEC3G, and CUL5
encode HIV-1 postentry cellular viral cofactors that have been described in recent research.
These miRs have been found to downregulate several genes (PCD4, CCL20, CHL1, CUL5
, TNK52, XIAP, TP53INP, and P3IK), most of which usually undergo DNA methylation in cervical cancer and regulate cell growth, proliferation, and apoptosis, mechanisms that are critical in HPV-related tumorigenesis.
Yan, "Downregulation of MicroRNA-145 caused by Hepatitis B Virus X protein promotes expression of CUL5
and contributes to pathogenesis of Hepatitis B virus-associated hepatocellular carcinoma," Cellular Physiology and Biochemistry, vol.
proved that renal edema, glomerular structure changes, and proteinuria were observed in Zebrafish after the CUL5 knockdown , suggesting the pivotal role of Cullin-5 in maintaining the physiological function of glomerular epithelial cells.
MicroRNA-19a and -19b regulate cervical carcinoma cell proliferation and invasion by targeting CUL5. Cancer Lett.
We observed positive correlations (absolute value > 0.15) with all ARGs, including PPIA (0.42), ZNRD1 (0.37), MYH9 (0.36), TSG101 (0.31), IDH1 (0.28), TRIM5a (0.17), and CUL5 (0.15), but not GML (-0.17) and NCOR2 (-0.31).
This variable highly correlated with the ARGs PPIA (0.92), CUL5 (0.51), TSG101 (0.48), IDH1 (0.17), and PECI (0.15), but not GML (-0.16), APOBEC3G (-0.17), MYH9 (-0.17), IL4 (-0.18), TLR9 (-0.18), CXCR1 (-0.25), HLA-C (-0.26), NCOR2 (-0.28), DC-SIGN (-0.29), and TLR8 (-0.36).
VHL is a component of the VHL elongin BC complex--composed of the proteins VHL, CUL2 or CUL5, RBX1, and elongin B/elongin C (elongins B and C are encoded by TCEB1 and TCEB2, resp.).
Our results indicate that, while VHL is disrupted in both PCC and RCC, other components of the VHL elongin BC complex, particularly RBX1 and CUL5, are significantly disrupted in PCC and their status might be an important clinical consideration in PCC.