留言板

尊敬的读者、作者、审稿人, 关于本刊的投稿、审稿、编辑和出版的任何问题, 您可以本页添加留言。我们将尽快给您答复。谢谢您的支持!

姓名
邮箱
手机号码
标题
留言内容
验证码

Disruptor of telomeric silencing 1-like (DOT1L) is involved in breast cancer metastasis via transcriptional regulation of MALAT1 and ZEB2

Yang Duan Xingyan Zhang Lihong Yang Xu Dong Zhanye Zheng Yiming Cheng Hao Chen Bei Lan Dengwen Li Jun Zhou Chenghao Xuan

Yang Duan, Xingyan Zhang, Lihong Yang, Xu Dong, Zhanye Zheng, Yiming Cheng, Hao Chen, Bei Lan, Dengwen Li, Jun Zhou, Chenghao Xuan. Disruptor of telomeric silencing 1-like (DOT1L) is involved in breast cancer metastasis via transcriptional regulation of MALAT1 and ZEB2[J]. Journal of Genetics and Genomics, 2019, 46(12): 591-594. doi: 10.1016/j.jgg.2019.11.008
Citation: Yang Duan, Xingyan Zhang, Lihong Yang, Xu Dong, Zhanye Zheng, Yiming Cheng, Hao Chen, Bei Lan, Dengwen Li, Jun Zhou, Chenghao Xuan. Disruptor of telomeric silencing 1-like (DOT1L) is involved in breast cancer metastasis via transcriptional regulation of MALAT1 and ZEB2[J]. Journal of Genetics and Genomics, 2019, 46(12): 591-594. doi: 10.1016/j.jgg.2019.11.008

doi: 10.1016/j.jgg.2019.11.008

Disruptor of telomeric silencing 1-like (DOT1L) is involved in breast cancer metastasis via transcriptional regulation of MALAT1 and ZEB2

More Information
  • [1] Dawson, M.A., Kouzarides, T., 2012. Cancer epigenetics: from mechanism to therapy. Cell 150, 12-27.
    [2] Duan, Y., Wu, X., Zhao, Q., Gao, J., Huo, D., Liu, X., Ye, Z., Dong, X., Fu, Z., Shang, Y., Xuan, C., 2016. DOT1L promotes angiogenesis through cooperative regulation of VEGFR2 with ETS-1. Oncotarget 7, 69674-69687.
    [3] Fan, Y., Shen, B., Tan, M., Mu, X., Qin, Y., Zhang, F., Liu, Y., 2014. TGF-beta-induced upregulation of malat1 promotes bladder cancer metastasis by associating with suz12. Clin Cancer Res 20, 1531-1541.
    [4] Fardi, M., Alivand, M., Baradaran, B., Farshdousti Hagh, M., Solali, S., 2019. The crucial role of ZEB2: From development to epithelial-to-mesenchymal transition and cancer complexity. Journal of cellular physiology.
    [5] Feng, Q., Wang, H., Ng, H.H., Erdjument-Bromage, H., Tempst, P., Struhl, K., Zhang, Y., 2002. Methylation of H3-lysine 79 is mediated by a new family of HMTases without a SET domain. Curr Biol 12, 1052-1058.
    [6] Fingerman, I.M., Li, H.C., Briggs, S.D., 2007. A charge-based interaction between histone H4 and Dot1 is required for H3K79 methylation and telomere silencing: identification of a new trans-histone pathway. Genes & development 21, 2018-2029.
    [7] Garraway, L.A., Lander, E.S., 2013. Lessons from the cancer genome. Cell 153, 17-37.
    [8] Gutschner, T., Hammerle, M., Eissmann, M., Hsu, J., Kim, Y., Hung, G., Revenko, A., Arun, G., Stentrup, M., Gross, M., Zornig, M., MacLeod, A.R., Spector, D.L., Diederichs, S., 2013. The noncoding RNA MALAT1 is a critical regulator of the metastasis phenotype of lung cancer cells. Cancer research 73, 1180-1189.
    [9] Imai, S., Armstrong, C.M., Kaeberlein, M., Guarente, L., 2000. Transcriptional silencing and longevity protein Sir2 is an NAD-dependent histone deacetylase. Nature 403, 795-800.
    [10] Katoh, M., Katoh, M., 2009. Integrative genomic analyses of ZEB2: Transcriptional regulation of ZEB2 based on SMADs, ETS1, HIF1alpha, POU/OCT, and NF-kappaB. Int J Oncol 34, 1737-1742.
    [11] Krivtsov, A.V., Feng, Z., Lemieux, M.E., Faber, J., Vempati, S., Sinha, A.U., Xia, X., Jesneck, J., Bracken, A.P., Silverman, L.B., Kutok, J.L., Kung, A.L., Armstrong, S.A., 2008. H3K79 methylation profiles define murine and human MLL-AF4 leukemias. Cancer Cell 14, 355-368.
    [12] Kruhlak, M.J., Celeste, A., Dellaire, G., Fernandez-Capetillo, O., Muller, W.G., McNally, J.G., Bazett-Jones, D.P., Nussenzweig, A., 2006. Changes in chromatin structure and mobility in living cells at sites of DNA double-strand breaks. The Journal of cell biology 172, 823-834.
    [13] Mei, S., Qin, Q., Wu, Q., Sun, H., Zheng, R., Zang, C., Zhu, M., Wu, J., Shi, X., Taing, L., Liu, T., Brown, M., Meyer, C.A., Liu, X.S., 2017. Cistrome Data Browser: a data portal for ChIP-Seq and chromatin accessibility data in human and mouse. Nucleic acids research 45, D658-D662.
    [14] Mueller, D., Bach, C., Zeisig, D., Garcia-Cuellar, M.P., Monroe, S., Sreekumar, A., Zhou, R., Nesvizhskii, A., Chinnaiyan, A., Hess, J.L., Slany, R.K., 2007. A role for the MLL fusion partner ENL in transcriptional elongation and chromatin modification. Blood 110, 4445-4454.
    [15] Nguyen, A.T., Zhang, Y., 2011. The diverse functions of Dot1 and H3K79 methylation. Genes & development 25, 1345-1358.
    [16] Okada, Y., Feng, Q., Lin, Y., Jiang, Q., Li, Y., Coffield, V.M., Su, L., Xu, G., Zhang, Y., 2005. hDOT1L links histone methylation to leukemogenesis. Cell 121, 167-178.
    [17] Sinh, N.D., Endo, K., Miyazawa, K., Saitoh, M., 2017. Ets1 and ESE1 reciprocally regulate expression of ZEB1/ZEB2, dependent on ERK1/2 activity, in breast cancer cells. Cancer Sci 108, 952-960.
    [18] Stein, E.M., Garcia-Manero, G., Rizzieri, D.A., Tibes, R., Berdeja, J.G., Savona, M.R., Jongen-Lavrenic, M., Altman, J.K., Thomson, B., Blakemore, S.J., Daigle, S.R., Waters, N.J., Suttle, A.B., Clawson, A., Pollock, R., Krivtsov, A., Armstrong, S.A., DiMartino, J., Hedrick, E., Lowenberg, B., Tallman, M.S., 2018. The DOT1L inhibitor pinometostat reduces H3K79 methylation and has modest clinical activity in adult acute leukemia. Blood 131, 2661-2669.
    [19] Strahl, B.D., Allis, C.D., 2000. The language of covalent histone modifications. Nature 403, 41-45.
    [20] Younesy, H., Nielsen, C.B., Lorincz, M.C., Jones, S.J., Karimi, M.M., Moller, T., 2016. ChAsE: chromatin analysis and exploration tool. Bioinformatics 32, 3324-3326.
  • 加载中
计量
  • 文章访问数:  87
  • HTML全文浏览量:  28
  • PDF下载量:  3
  • 被引次数: 0
出版历程
  • 收稿日期:  2019-11-23
  • 录用日期:  2019-11-25
  • 网络出版日期:  2019-12-17
  • 刊出日期:  2019-12-20

目录

    /

    返回文章
    返回