Редактирование: CBX8

Chromobox protein homolog 8 (Polycomb 3 homolog) (Pc3) (hPc3) (Rectachrome 1) [PC3] [RC1]

==Publications==

{{medline-entry
|title=[[PIM1]]-catalyzed [[CBX8]] phosphorylation promotes the oncogene-induced senescence of human diploid fibroblast.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/29763603
|abstract=The proto-oncogene [[PIM1]] encodes Ser/Thr kinase and regulates cell growth, differentiation and apoptosis. However, more and more studies including ours have found that [[PIM1]] can induce senescence in normal human diploid fibroblasts and behave as a tumor suppressor. But the relevant molecular mechanism of this process is not yet clear. It has been reported that Chromobox homolog 8 ([[CBX8]]) binds directly to INK4A as a transcriptional repressor, thereby suppressing stress-induced senescence. Here we report that [[PIM1]] can phosphorylate [[CBX8]] to promote its degradation, thereby up-regulating p16, during [[PIM1]]-induced cell senescence. Overexpression of [[CBX8]] can inhibit [[PIM1]]-induced cell senescence. These data suggest that to promote [[CBX8]] degradation may be an important molecular mechanism of [[PIM1]]-induced cell senescence.
|mesh-terms=* Cell Line
* Cell Proliferation
* Cellular Senescence
* Down-Regulation
* Fibroblasts
* Genes, p16
* HEK293 Cells
* Humans
* Phosphorylation
* Polycomb Repressive Complex 1
* Proteolysis
* Proto-Oncogene Proteins c-pim-1
* Up-Regulation
|keywords=* CBX8
* PIM1
* Phosphorylation
* Senescence
|full-text-url=https://sci-hub.do/10.1016/j.bbrc.2018.05.070
}}
{{medline-entry
|title=[[CBX8]] antagonizes the effect of Sirtinol on premature senescence through the AKT-RB-[[E2F1]] pathway in K562 leukemia cells.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/26718407
|abstract=Although tyrosine kinase inhibitor (TKI) therapies are highly effective in the treatment of chronic myeloid leukemia (CML), frequent recurrence limits their usage and demands new approaches for CML therapy. Stress-induced premature senescence (SIPS) is considered a potential anticancer treatment, but the underlying mechanism remains elusive. Here, we report that Sirtinol, a known [[SIRT1]] inhibitor, induces premature senescence and growth arrest in K562 CML cells. Chromobox homolog 8 ([[CBX8]]) suppresses the Sirtinol-induced premature senescence, which is reversed by [[CBX8]] knockdown. Upon Sirtinol treatment, the phosphorylation of [[AKT1]], p27KIP1 and RB is severely downregulated. However, [[CBX8]] overexpression enhances phosphorylation and, thereby, promotes the transcriptional activity of [[E2F1]], both of which are impaired upon CBX depletion. These data suggest that [[CBX8]] modulates SIPS through the RB-[[E2F1]] pathway in CML cells and provide important insight into its application in CML treatment. 
|mesh-terms=* Antineoplastic Agents
* Benzamides
* Cell Cycle Checkpoints
* Cellular Senescence
* Drug Antagonism
* E2F1 Transcription Factor
* Humans
* K562 Cells
* Leukemia, Myelogenous, Chronic, BCR-ABL Positive
* Naphthols
* Oncogene Protein v-akt
* Polycomb Repressive Complex 1
* Retinoblastoma Protein
* Signal Transduction
|keywords=* CBX8
* Leukemia
* Premature senescence
* RB-E2F1
* SIRT1
|full-text-url=https://sci-hub.do/10.1016/j.bbrc.2015.12.070
}}