| General information | Literature | Expression | Regulation | Mutation | Homolog | Interaction |
Basic Information | |
|---|---|
Gene ID | 5970 |
Name | RELA |
Synonymous | v-rel avian reticuloendotheliosis viral oncogene homolog A;RELA;v-rel avian reticuloendotheliosis viral oncogene homolog A |
Definition | NF-kappa-B p65delta3|nuclear factor NF-kappa-B p65 subunit|nuclear factor of kappa light polypeptide gene enhancer in B-cells 3|transcription factor p65|v-rel reticuloendotheliosis viral oncogene homolog A |
Position | 11q13 |
Gene type | protein-coding |
Title | Abstract |
| Silencing of the DEK gene induces apoptosis and senescence in CaSki cervical carcinoma cells via the up-regulation of NF-kappaB p65. | The human DEK proto-oncogene has been found to play an important role in autoimmune disease, viral infection and human carcinogenesis. Although it is transcriptionally up-regulated in cervical cancer, its intracellular function and regulation is still unexplored. In the present study, DEK and IkappaBalpha [inhibitor of NF-kappaB (nuclear factor kappaB) alpha] shRNAs (short hairpin RNAs) were constructed and transfected into CaSki cells using Lipofectamine. The stable cell line CaSki-DEK was obtained after G418 selection. CaSki-IkappaB cells were observed at 48 h after psiRNA-IkappaB transfection. The inhibitory efficiency of shRNAs were detected by RT (reverse transcription)-PCR and Western blot analysis. The proliferation activity of cells were measured using an MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-2H-tetrazolium bromide] assay, cell apoptosis was measured using an Annexin V/PI (propidium iodide) kit, the cell cycle was analysed by flow cytometry and cell senescence was detected using senescence beta-galactosidase staining. The intracellular expression of NF-kappaB p65 protein was studied by cytochemistry. The expression levels of NF-kappaB p65, p50, c-Rel, IkappaBalpha and phospho-IkappaBalpha protein were analysed by immunoblotting in whole-cell lysates, cytosolic fractions and nuclear extracts. The protein expression and activity of p38 and JNK (c-Jun N-terminal kinase) were also assayed. In addition, the NF-kappaB p65 DNA-binding activity was measured by ELISA. Following the silencing of DEK and IkappaBalpha, cell proliferation was inhibited, apoptosis was increased, the cell cycle was blocked in the G0/G1-phase with a corresponding decrease in the G2/M-phase, and cell senescence was induced. ALL of these effects may be related to the up-regulation of NF-kappaB p65 expression and its nuclear translocation. |