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CBX8
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==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 }}
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