The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.
Global H3K27 trimethylation and EZH2 abundance in breast tumor subtypes
Open accessAbstract
Polycomb repressive complex 2 (PRC2) and its core member enhancer of zeste homolog 2 (EZH2) mediate the epigenetic gene silencing mark: trimethylation of lysine 27 on histone 3 (H3K27me3). H3K27me3 is characteristic of the chromatin at genes involved in developmental regulation in undifferentiated cells. Overexpression of EZH2 has been found in several cancer types such as breast, prostate, melanoma and bladder cancer. Moreover, overexpression is associated with highly proliferative and aggressive types of breast and prostate tumors. We have analyzed the abundance of EZH2 and H3K27me3 using immunohistochemistry in two large and well‐characterized breast tumor data sets encompassing more than 400 tumors. The results have been analyzed in relation to the molecular subtypes of breast tumors (basal‐like, luminal A, luminal B, HER2‐enriched and normal‐like), as well as in subtypes defined by clinical markers (triple negative, ER+/HER2−/Ki67low, ER+/HER2−/Ki67high and HER2+), and were validated in representative breast cancer cell lines by western blot. We found significantly different expression of both EZH2 and H3K27me3 across all subtypes with high abundance of EZH2 in basal‐like, triple negative and HER2‐enriched tumors, and high H3K27me3 in luminal A, HER2‐enriched and normal‐like tumors. Intriguingly, the two markers show an inverse correlation, particularly for the basal‐like and triple negative tumors. Consequently, high expression of EZH2 was associated with poor distant disease‐free survival whereas high expression of H3K27me3 was associated with better survival. Additionally, none of 182 breast tumors was found to carry a previously described EZH2 mutation affecting Tyr641. Our observation that increased expression of EZH2 does not necessarily correlate with increased abundance of H3K27me3 supports the idea that EZH2 can have effects beyond epigenetic silencing of target genes in breast cancer.
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Cites
The Polycomb complex PRC2 and its mark in life
Margueron, R., & Reinberg, D. (2011) · Nature · doi:10.1038/nature09784 · Cited by 3,347
The polycomb group protein EZH2 is involved in progression of prostate cancer
Varambally, S., Dhanasekaran, S. M., Zhou, M., Barrette, T. R., Kumar-Sinha, C., Sanda, M. G., Ghosh, D., Pienta, K. J., Sewalt, R. G. A. B., Otte, A. P., et al. (2002) · Nature · doi:10.1038/nature01075 · Cited by 2,717
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kConFab, Lim, E., Vaillant, F., Wu, D., Forrest, N. C., Pal, B., Hart, A. H., Asselin-Labat, M.-L., Gyorki, D. E., Ward, T., et al. (2009) · Nature Medicine · doi:10.1038/nm.2000 · Cited by 1,492 · cited 1×
“This is consistent with the hypothesis of basal-like cancers having a more progenitor-like cell origin than luminal tumors (Lim et al., 2009).”
ResultSchlesinger, Y., Straussman, R., Keshet, I., Farkash, S., Hecht, M., Zimmerman, J., Eden, E., Yakhini, Z., Ben-Shushan, E., Reubinoff, B. E., et al. (2007) · Nature Genetics · doi:10.1038/ng1950 · Cited by 1,226
EZH2 is downstream of the pRB-E2F pathway, essential for proliferation and amplified in cancer.
Bracken, A. P., Pasini, D., Capra, M., Prosperini, E., Colli, E., & Helin, K. (2003) · The EMBO Journal · doi:10.1093/emboj/cdg542 · Cited by 1,196
Ohm, J. E., McGarvey, K. M., Yu, X., Cheng, L., Schuebel, K. E., Cope, L., Mohammad, H. P., Chen, W., Daniel, V. C., Yu, W., et al. (2007) · Nature Genetics · doi:10.1038/ng1972 · Cited by 1,130
Polycomb Group Protein Ezh2 Controls Actin Polymerization and Cell Signaling
Su, I.-H., Dobenecker, M.-W., Dickinson, E., Oser, M., Basavaraj, A., Marqueron, R., Viale, A., Reinberg, D., Wülfing, C., & Tarakhovsky, A. (2005) · Cell · doi:10.1016/j.cell.2005.02.029 · Cited by 365
Novel homo- and hemizygous mutations in EZH2 in myeloid malignancies
Makishima, H., Jankowska, A. M., Tiu, R. V., Szpurka, H., Sugimoto, Y., Hu, Z., Saunthararajah, Y., Guinta, K., Keddache, M. A., Putnam, P., et al. (2010) · Leukemia · doi:10.1038/leu.2010.167 · Cited by 179
Cited by
Stem cell programs in cancer initiation, progression, and therapy resistance
Huang, T., Song, X., Xu, D., Tiek, D., Goenka, A., Wu, B., Sastry, N., Hu, B., & Cheng, S.-Y. (2020) · Theranostics · doi:10.7150/thno.41648 · Cited by 524
Therapeutic Implications of Cellular Heterogeneity and Plasticity in Breast Cancer
Brooks, M. D., Burness, M. L., & Wicha, M. S. (2015) · Cell Stem Cell · doi:10.1016/j.stem.2015.08.014 · Cited by 374
EZH2-H3K27me3 mediated KRT14 upregulation promotes TNBC peritoneal metastasis
Verma, A., Singh, A., Singh, M. P., Nengroo, M. A., Saini, K. K., Satrusal, S. R., Khan, M. A., Chaturvedi, P., Sinha, A., Meena, S., et al. (2022) · Nature Communications · doi:10.1038/s41467-022-35059-x · Cited by 148
Lkb1 inactivation drives lung cancer lineage switching governed by Polycomb Repressive Complex 2
Zhang, H., Fillmore Brainson, C., Koyama, S., Redig, A. J., Chen, T., Li, S., Gupta, M., Garcia-de-Alba, C., Paschini, M., Herter-Sprie, G. S., et al. (2017) · Nature Communications · doi:10.1038/ncomms14922 · Cited by 127
Mahara, S., Lee, P. L., Feng, M., Tergaonkar, V., Chng, W. J., & Yu, Q. (2016) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1602079113 · Cited by 87
Metadata
- Authors
- Holm, K., Grabau, D., Lövgren, K., Aradottir, S., Gruvberger-Saal, S., Howlin, J., Saal, L. H., Ethier, S. P., Bendahl, P.-O., Stål, O., Malmström, P., Fernö, M., Rydén, L., Hegardt, C., Borg, Å., & Ringnér, M.
- Venue
- Molecular Oncology
- Publisher
- Wiley
- Published
- 2012-06-20
- Volume
- 6
- Issue
- 5
- Pages
- 494-506
- ISSN
- 1574-7891 (ISSN-L)
- 1878-0261
- OpenAlex
- W2118203903
- Cited by
- 161
- References
- 9
- FWCI
- 4.76
- Type
- journal article
- Language
- en
- Open access
- green
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- Holm, K., Grabau, D., Lövgren, K., Aradottir, S., Gruvberger-Saal, S., Howlin, J., Saal, L. H., Ethier, S. P., Bendahl, P.-O., Stål, O., Malmström, P., Fernö, M., Rydén, L., Hegardt, C., Borg, Å., & Ringnér, M. (2012). Global H3K27 trimethylation and EZH2 abundance in breast tumor subtypes. Molecular Oncology. https://doi.org/10.1016/j.molonc.2012.06.002
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