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Gene Review

BMI1  -  BMI1 proto-oncogene, polycomb ring finger

Homo sapiens

Synonyms: FLVI2/BMI1, PCGF4, Polycomb complex protein BMI-1, Polycomb group RING finger protein 4, RING finger protein 51, ...
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Disease relevance of BMI1

  • They also colocalize with BMI1 in interphase nuclei of U-2 OS human osteosarcoma and SW480 human colorectal adenocarcinoma cells [1].
  • CALM-AF10+ T-ALL expression profiles are characterized by overexpression of HOXA and BMI1 oncogenes [2].
  • We also demonstrate linked overexpression of BMI1 and patched (PTCH), suggestive of SHH pathway activation, in a substantial fraction of primary human medulloblastomas [3].
  • Changes in expression associated with tumoral transformation have been found for BMI1 and RNF2, which exhibited increased expression in a large series of tumors, including gastrointestinal tumors, pituitary and parathyroid adenomas, and lymphomas, compared with their expression in normal-cell counterparts [4].
  • The high level of expression of BMI1 protein observed in mantle-cell lymphomas and pituitary adenomas is associated in some cases with amplification of BMI1 locus [4].
  • In a cohort of 64 CML patients, the level of BMI1 at diagnosis correlated with time to transformation to blast crisis, and the combination of low BMI1 and high proteinase-3 expression was associated in multivariate analysis with an improved overall survival (P = .001) [5].

High impact information on BMI1

  • The HPC/HPH PcG complex contains the human polycomb 2 (HPC2; ref. 11), human polyhomeotic (HPH), BMI1 (ref. 13 ) and RING1 (refs 14, 15) proteins [6].
  • Here, we demonstrate that Polycomb genes EZH2 and BMI1 repress p16 expression in human and mouse primary cells, but not in cells deficient for pRB protein function [7].
  • Genetic studies have demonstrated that Bmi1 promotes cell proliferation and stem cell self-renewal with a correlative decrease of p16(INK4a) expression [7].
  • Together, these findings identify E4F1 as a key modulator of BMI1 activity in primitive hematopoietic cells [8].
  • E4F1: a novel candidate factor for mediating BMI1 function in primitive hematopoietic cells [8].

Biological context of BMI1

  • Chromatin-association of the Polycomb group protein BMI1 is cell cycle-regulated and correlates with its phosphorylation status [9].
  • In primary and tumor cells, nuclear BMI1 shows a fine-grain distribution over chromatin, usually dense in interphase nuclei and significantly weaker along mitotic chromosomes [9].
  • BMI1 controls cellular proliferation through suppression of the tumor suppressors encoded by the CDKN2A locus [2].
  • BMI1 gene expression was significantly down-regulated with increasing donor age, whereas no striking age differences were observed for Ki67 [10].
  • Despite a significant overlap in dosage-sensitive homeotic phenotypes and co-repression of a similar set of Hox genes, genetic analysis implicated eed and Bmi1 in parallel pathways, which converge at the level of Hox gene regulation [11].

Anatomical context of BMI1


Associations of BMI1 with chemical compounds

  • We also demonstrated that loss of BMI1 was more effective in suppressing cancer cell growth than retinoid-treatment, and surviving cancer cells showed significantly reduced tumorigenicity [15].

Physical interactions of BMI1


Enzymatic interactions of BMI1

  • Here, we report that the E3 ubiquitin ligase consisting of SPOP and CULLIN3 is able to ubiquitinate the Polycomb group protein BMI1 and the variant histone MACROH2A [17].

Regulatory relationships of BMI1


Other interactions of BMI1

  • Association of BMI1 with polycomb bodies is dynamic and requires PRC2/EZH2 and the maintenance DNA methyltransferase DNMT1 [18].
  • Polycomb protein Bmi1, which is a potent negative regulator of the p16INK4 gene, suppresses senescence in primary cells and is overexpressed in various cancers [13].
  • Here, we investigate the kinetic properties of the binding of one of the PRC1 core components, BMI1, with PcG bodies [18].
  • In both primary and tumor cell lines a marked cell cycle-regulation of Pc-G-chromatin interaction is observed: nuclear BMI1-staining dissipates in late S phase and is re-established early in G(1)-phase [9].
  • The E2F6 transcription factor is a component of the mammalian Bmi1-containing polycomb complex [19].

Analytical, diagnostic and therapeutic context of BMI1


  1. Identification and characterization of interactions between the vertebrate polycomb-group protein BMI1 and human homologs of polyhomeotic. Gunster, M.J., Satijn, D.P., Hamer, K.M., den Blaauwen, J.L., de Bruijn, D., Alkema, M.J., van Lohuizen, M., van Driel, R., Otte, A.P. Mol. Cell. Biol. (1997) [Pubmed]
  2. CALM-AF10+ T-ALL expression profiles are characterized by overexpression of HOXA and BMI1 oncogenes. Dik, W.A., Brahim, W., Braun, C., Asnafi, V., Dastugue, N., Bernard, O.A., van Dongen, J.J., Langerak, A.W., Macintyre, E.A., Delabesse, E. Leukemia (2005) [Pubmed]
  3. Bmi1 is essential for cerebellar development and is overexpressed in human medulloblastomas. Leung, C., Lingbeek, M., Shakhova, O., Liu, J., Tanger, E., Saremaslani, P., Van Lohuizen, M., Marino, S. Nature (2004) [Pubmed]
  4. Variability in the expression of polycomb proteins in different normal and tumoral tissues. A pilot study using tissue microarrays. Sánchez-Beato, M., Sánchez, E., González-Carreró, J., Morente, M., Díez, A., Sánchez-Verde, L., Martín, M.C., Cigudosa, J.C., Vidal, M., Piris, M.A. Mod. Pathol. (2006) [Pubmed]
  5. The polycomb group BMI1 gene is a molecular marker for predicting prognosis of chronic myeloid leukemia. Mohty, M., Yong, A.S., Szydlo, R.M., Apperley, J.F., Melo, J.V. Blood (2007) [Pubmed]
  6. Transcriptional repression mediated by the human polycomb-group protein EED involves histone deacetylation. van der Vlag, J., Otte, A.P. Nat. Genet. (1999) [Pubmed]
  7. pRB family proteins are required for H3K27 trimethylation and Polycomb repression complexes binding to and silencing p16INK4a tumor suppressor gene. Kotake, Y., Cao, R., Viatour, P., Sage, J., Zhang, Y., Xiong, Y. Genes Dev. (2007) [Pubmed]
  8. E4F1: a novel candidate factor for mediating BMI1 function in primitive hematopoietic cells. Chagraoui, J., Niessen, S.L., Lessard, J., Girard, S., Coulombe, P., Sauvageau, M., Meloche, S., Sauvageau, G. Genes Dev. (2006) [Pubmed]
  9. Chromatin-association of the Polycomb group protein BMI1 is cell cycle-regulated and correlates with its phosphorylation status. Voncken, J.W., Schweizer, D., Aagaard, L., Sattler, L., Jantsch, M.F., van Lohuizen, M. J. Cell. Sci. (1999) [Pubmed]
  10. p16 is a robust in vivo biomarker of cellular aging in human skin. Ressler, S., Bartkova, J., Niederegger, H., Bartek, J., Scharffetter-Kochanek, K., Jansen-Dürr, P., Wlaschek, M. Aging Cell (2006) [Pubmed]
  11. Juxtaposed Polycomb complexes co-regulate vertebral identity. Kim, S.Y., Paylor, S.W., Magnuson, T., Schumacher, A. Development (2006) [Pubmed]
  12. Abnormal PcG protein expression in Hodgkin's lymphoma. Relation with E2F6 and NFkappaB transcription factors. Sánchez-Beato, M., Sánchez, E., García, J.F., Pérez-Rosado, A., Montoya, M.C., Fraga, M., Artiga, M.J., Navarrete, M., Abraira, V., Morente, M., Esteller, M., Koseki, H., Vidal, M., Piris, M.A. J. Pathol. (2004) [Pubmed]
  13. Dysregulated expression of stem cell factor bmi1 in precancerous lesions of the gastrointestinal tract. Tateishi, K., Ohta, M., Kanai, F., Guleng, B., Tanaka, Y., Asaoka, Y., Tada, M., Seto, M., Jazag, A., Lianjie, L., Okamoto, M., Isayama, H., Tada, M., Yoshida, H., Kawabe, T., Omata, M. Clin. Cancer Res. (2006) [Pubmed]
  14. BMI-1 is highly expressed in M0-subtype acute myeloid leukemia. Sawa, M., Yamamoto, K., Yokozawa, T., Kiyoi, H., Hishida, A., Kajiguchi, T., Seto, M., Kohno, A., Kitamura, K., Itoh, Y., Asou, N., Hamajima, N., Emi, N., Naoe, T. Int. J. Hematol. (2005) [Pubmed]
  15. Loss of the human polycomb group protein BMI1 promotes cancer-specific cell death. Liu, L., Andrews, L.G., Tollefsbol, T.O. Oncogene (2006) [Pubmed]
  16. Bmi1 cooperates with Dnmt1-associated protein 1 in gene silencing. Negishi, M., Saraya, A., Miyagi, S., Nagao, K., Inagaki, Y., Nishikawa, M., Tajima, S., Koseki, H., Tsuda, H., Takasaki, Y., Nakauchi, H., Iwama, A. Biochem. Biophys. Res. Commun. (2007) [Pubmed]
  17. Stable X chromosome inactivation involves the PRC1 Polycomb complex and requires histone MACROH2A1 and the CULLIN3/SPOP ubiquitin E3 ligase. Hernández-Muñoz, I., Lund, A.H., van der Stoop, P., Boutsma, E., Muijrers, I., Verhoeven, E., Nusinow, D.A., Panning, B., Marahrens, Y., van Lohuizen, M. Proc. Natl. Acad. Sci. U.S.A. (2005) [Pubmed]
  18. Association of BMI1 with polycomb bodies is dynamic and requires PRC2/EZH2 and the maintenance DNA methyltransferase DNMT1. Hernández-Muñoz, I., Taghavi, P., Kuijl, C., Neefjes, J., van Lohuizen, M. Mol. Cell. Biol. (2005) [Pubmed]
  19. The E2F6 transcription factor is a component of the mammalian Bmi1-containing polycomb complex. Trimarchi, J.M., Fairchild, B., Wen, J., Lees, J.A. Proc. Natl. Acad. Sci. U.S.A. (2001) [Pubmed]
  20. Histological type of oncogenity and expression of cell cycle genes in tumor cells from human mesenchymal stem cells. Jiang, R., Xu, W., Zhu, W., Chen, M., Qian, H., Qiao, C., Yang, H., Wang, X., Chen, Y. Oncol. Rep. (2006) [Pubmed]
  21. Characterization and chromosomal localization of the human proto-oncogene BMI-1. Alkema, M.J., Wiegant, J., Raap, A.K., Berns, A., van Lohuizen, M. Hum. Mol. Genet. (1993) [Pubmed]
  22. BMI-1 gene amplification and overexpression in hematological malignancies occur mainly in mantle cell lymphomas. Beà, S., Tort, F., Pinyol, M., Puig, X., Hernández, L., Hernández, S., Fernandez, P.L., van Lohuizen, M., Colomer, D., Campo, E. Cancer Res. (2001) [Pubmed]
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