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

doi:10.1016/j.jgg.2019.11.008

Volume 46 Issue 12

Dec. 2019

Turn off MathJax

Article Contents

Article Navigation > Journal of Genetics and Genomics > 2019 > 46(12): 591-594

PDF( 862 KB)

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

doi: 10.1016/j.jgg.2019.11.008

Yang Duan^{1, 2},
Xingyan Zhang³,
Lihong Yang⁴,
Xu Dong⁵,
Zhanye Zheng⁶,
Yiming Cheng⁷,
Hao Chen⁸,
Bei Lan⁹,
Dengwen Li¹⁰,
Jun Zhou^{11, 12},
Chenghao Xuan¹³

1
Tianjin Key Laboratory of Medical Epigenetics, Key Laboratory of Breast Cancer Prevention and Therapy (Ministry of Education), Tianjin Key Laboratory of Spine and Spinal Cord, Department of Biochemistry and Molecular Biology, Tianjin Medical University, Tianjin, 300070, China
2
Department of Gynecology, Tianjin Medical University NanKai Hospital, Tianjin 300100, China
3
Tianjin Key Laboratory of Medical Epigenetics, Key Laboratory of Breast Cancer Prevention and Therapy (Ministry of Education), Tianjin Key Laboratory of Spine and Spinal Cord, Department of Biochemistry and Molecular Biology, Tianjin Medical University, Tianjin, 300070, China
4
Department of Genetics and Cell Biology, College of Life Sciences, Nankai University, Tianjin 300071, China
5
Tianjin Key Laboratory of Medical Epigenetics, Key Laboratory of Breast Cancer Prevention and Therapy (Ministry of Education), Tianjin Key Laboratory of Spine and Spinal Cord, Department of Biochemistry and Molecular Biology, Tianjin Medical University, Tianjin, 300070, China
6
Department of Pharmacology, Tianjin Medical University, Tianjin, 300070, China
7
Tianjin Key Laboratory of Medical Epigenetics, Key Laboratory of Breast Cancer Prevention and Therapy (Ministry of Education), Tianjin Key Laboratory of Spine and Spinal Cord, Department of Biochemistry and Molecular Biology, Tianjin Medical University, Tianjin, 300070, China
8
Tianjin Key Laboratory of Medical Epigenetics, Key Laboratory of Breast Cancer Prevention and Therapy (Ministry of Education), Tianjin Key Laboratory of Spine and Spinal Cord, Department of Biochemistry and Molecular Biology, Tianjin Medical University, Tianjin, 300070, China
9
Tianjin Key Laboratory of Medical Epigenetics, Key Laboratory of Breast Cancer Prevention and Therapy (Ministry of Education), Tianjin Key Laboratory of Spine and Spinal Cord, Department of Biochemistry and Molecular Biology, Tianjin Medical University, Tianjin, 300070, China
10
Department of Genetics and Cell Biology, College of Life Sciences, Nankai University, Tianjin 300071, China
11
Department of Genetics and Cell Biology, College of Life Sciences, Nankai University, Tianjin 300071, China
12
Institute of Biomedical Sciences, College of Life Sciences, Shandong Normal University, Shandong 250014, China
13
Tianjin Key Laboratory of Medical Epigenetics, Key Laboratory of Breast Cancer Prevention and Therapy (Ministry of Education), Tianjin Key Laboratory of Spine and Spinal Cord, Department of Biochemistry and Molecular Biology, Tianjin Medical University, Tianjin, 300070, China

More Information

Corresponding author: E-mail address: chenghaoxuan@tmu.edu.cn (Chenghao Xuan)
Received Date: 2019-11-23
Accepted Date: 2019-11-25

Available Online: 2019-12-17

Publish Date: 2019-12-20

Abstract

FullText(HTML)

References(20)

References

[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.