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Tet methylcytosine dioxygenase 1

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Template:PBB Ten-eleven translocation methylcytosine dioxygenase 1 (TET1) is a member of the TET family of enzymes that in humans is encoded by the TET1 gene.[1][2] It was first discovered in a 61 year old patient with a rare variation of t(10;11)(q22;q23) acute myeloid leukemiaa(AML)s a zinc-finger binding protein (specifically on the CXXC domain) that fuses to the gene MLL.[3] Another study confirmed that this protein was a translocation partner of MLL in an 8 year old patient with t(10;11)(q22;q23) AML and named the protein Ten-Eleven Translocation 1.[4]

TET1 catalyzes the conversion of the modified DNA base 5-methylcytosine (5-mC) to 5-hydroxymethylcytosine (5-hmC).[5] TET1 produces 5-hmC by oxidation of 5-mC in an iron and alpha-ketoglutarate dependent manner.[6] The conversion of 5-mC to 5-hmC has been proposed as the initial step of active DNA demethylation in mammals.[6] Additionally, downgrading TET1 has decreased levels of 5-formylcytosine (5-fC)  and 5-carboxylcytosine (5-caC) in both cell cultures and mice.[7]

TET1 appears to facilitate nuclear reprogramming of somatic cells to iPS cells.[8] [9] Patients with schizophrenia or bipolar disorder have shown increased levels of TET1 mRNA and protein expression in the inferior parietal lobule, indicating these diseases may be caused by mistakes in gene expression regulation.[10]

Colon, breast, prostate and liver tumors have significantly reduced levels of TET1 compared to the healthy colon cells and normal epithelial colon cells with downgraded TET1 levels have greater levels of proliferation.[11][12][13][14] Additionally, increasing TET1 expression levels in colon cancer cells decreased cell proliferation in both cell cultures and mice through demethylation of promoters of the WNT signaling pathway.[12].

Breast cancer cell lines with silenced TET1 expression have increased rates of invasion and breast cancers that spread to the lymph nodes are characterized by lower TET1 levels.[15] TET1 levels could be used to detect breast cancer metastasis.[15] A histone deacetylase inhibitor Trichostatin A increased levels of TET1 in breast cancer tissues but was a less effective tumor suppressor in patients with low TET1 expression.[16] Breast cancer patients with high TET1 levels had significantly higher survival probabilities than patients with low TET1 levels.[14]

Degradation of TET1 in hypoxnia-induced EMT lung cancer cells led to reduced metastasis rates and cells.[17] Healthy cells transitioning to cancer cells have decreased levels of TET1 but decreasing TET1 expression does not lead to malignancy.[18] Cancer cells using the KRAS pathway had decreased invasive potential after reintroducing TET1, likewise downgrading KRAS increased TET1 levels.[19]

References

  1. ^ "Entrez Gene: Tet methylcytosine dioxygenase 1". Retrieved 2012-07-26.
  2. ^ Coulter JB, O'Driscoll CM, Bressler JP (October 2013). "Hydroquinone increases 5-hydroxymethylcytosine formation through ten eleven translocation 1 (TET1) 5-methylcytosine dioxygenase". The Journal of Biological Chemistry. 288 (40): 28792–800. doi:10.1074/jbc.M113.491365. PMC 3789975. PMID 23940045.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  3. ^ Ono, Ryoichi; Taki, Tomohiko; Taketani, Takeshi; Taniwaki, Masafumi; Kobayashi, Hajime; Hayashi, Yasuhide (2002-07-15). "LCX, Leukemia-associated Protein with a CXXC Domain, Is Fused to MLL in Acute Myeloid Leukemia with Trilineage Dysplasia Having t(10;11)(q22;q23)". Cancer Research. 62 (14): 4075–4080. ISSN 0008-5472. PMID 12124344.
  4. ^ Lorsbach, R. B.; Moore, J.; Mathew, S.; Raimondi, S. C.; Mukatira, S. T.; Downing, J. R. (2003-03-06). "TET1, a member of a novel protein family, is fused to MLL in acute myeloid leukemia containing the t(10;11)(q22;q23)". Leukemia. 17 (3): 637–641. doi:10.1038/sj.leu.2402834. ISSN 0887-6924.
  5. ^ Tahiliani M, Koh KP, Shen Y, Pastor WA, Bandukwala H, Brudno Y, Agarwal S, Iyer LM, Liu DR, Aravind L, Rao A (May 2009). "Conversion of 5-methylcytosine to 5-hydroxymethylcytosine in mammalian DNA by MLL partner TET1". Science. 324 (5929): 930–5. doi:10.1126/science.1170116. PMC 2715015. PMID 19372391.
  6. ^ a b Ito S, Shen L, Dai Q, Wu SC, Collins LB, Swenberg JA, He C, Zhang Y (September 2011). "Tet proteins can convert 5-methylcytosine to 5-formylcytosine and 5-carboxylcytosine". Science. 333 (6047): 1300–3. doi:10.1126/science.1210597. PMC 3495246. PMID 21778364.
  7. ^ Ito S, Shen L, Dai Q, Wu SC, Collins LB, Swenberg JA, He C, Zhang Y (September 2011). "Tet proteins can convert 5-methylcytosine to 5-formylcytosine and 5-carboxylcytosine". Science. 333 (6047): 1300–3. doi:10.1126/science.1210597. PMC 3495246. PMID 21778364.
  8. ^ Pera MF (December 2013). "Epigenetics, vitamin supplements and cellular reprogramming". Nature Genetics. 45 (12): 1412–3. doi:10.1038/ng.2834. PMID 24270443.
  9. ^ Chen J, Gao Y, Huang H, Xu K, Chen X, Jiang Y, Li H, Gao S, Tao Y, Wang H, Zhang Y, Wang H, Cai T, Gao S (March 2015). "The combination of Tet1 with Oct4 generates high-quality mouse-induced pluripotent stem cells". Stem Cells. 33 (3): 686–98. doi:10.1002/stem.1879. PMID 25331067.
  10. ^ Dong E, Gavin DP, Chen Y, Davis J (2012-09-01). "Upregulation of TET1 and downregulation of APOBEC3A and APOBEC3C in the parietal cortex of psychotic patients". Translational Psychiatry. 2 (9): e159. doi:10.1038/tp.2012.86. PMC 3565208. PMID 22948384.
  11. ^ Yang H, Liu Y, Bai F, Zhang JY, Ma SH, Liu J, Xu ZD, Zhu HG, Ling ZQ, Ye D, Guan KL, Xiong Y (January 2013). "Tumor development is associated with decrease of TET gene expression and 5-methylcytosine hydroxylation". Oncogene. 32 (5): 663–9. doi:10.1038/onc.2012.67. PMC 3897214. PMID 22391558.
  12. ^ a b Neri F, Dettori D, Incarnato D, Krepelova A, Rapelli S, Maldotti M, Parlato C, Paliogiannis P, Oliviero S (August 2015). "TET1 is a tumour suppressor that inhibits colon cancer growth by derepressing inhibitors of the WNT pathway". Oncogene. 34 (32): 4168–76. doi:10.1038/onc.2014.356. PMID 25362856.
  13. ^ Liu, Chungang; Liu, Limei; Chen, Xuejiao; Shen, Junjie; Shan, Juanjuan; Xu, Yanmin; Yang, Zhi; Wu, Lin; Xia, Feng (2013-05-09). "Decrease of 5-Hydroxymethylcytosine Is Associated with Progression of Hepatocellular Carcinoma through Downregulation of TET1". PLoS ONE. 8 (5). doi:10.1371/journal.pone.0062828. ISSN 1932-6203. PMC 3650038. PMID 23671639.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  14. ^ a b Hsu, Chih-Hung; Peng, Kai-Lin; Kang, Ming-Lun; Chen, Yi-Ren; Yang, Yu-Chih; Tsai, Chin-Hsien; Chu, Chi-Shuen; Jeng, Yung-Ming; Chen, Yen-Ting (2012-09-27). "TET1 Suppresses Cancer Invasion by Activating the Tissue Inhibitors of Metalloproteinases". Cell Reports. 2 (3): 568–579. doi:10.1016/j.celrep.2012.08.030. ISSN 2211-1247. PMID 22999938.
  15. ^ a b Sang, Yi; Cheng, Chun; Tang, Xiao-Feng; Zhang, Mei-Fang; Lv, Xiao-Bin (2015-01-01). "Hypermethylation of TET1 promoter is a new diagnosic marker for breast cancer metastasis". Asian Pacific journal of cancer prevention: APJCP. 16 (3): 1197–1200. ISSN 1513-7368. PMID 25735355.
  16. ^ "TET1 partially mediates HDAC inhibitor-induced suppression of breast cancer invasion". www.spandidos-publications.com. Retrieved 2016-04-07.
  17. ^ Tsai, Ya-Ping; Chen, Hsiao-Fan; Chen, Sung-Yuan; Cheng, Wei-Chung; Wang, Hsei-Wei; Shen, Zih-Jie; Song, Chunxiao; Teng, Shu-Chun; He, Chuan (2014-01-01). "TET1 regulates hypoxia-induced epithelial-mesenchymal transition by acting as a co-activator". Genome Biology. 15 (12). doi:10.1186/s13059-014-0513-0. ISSN 1465-6906. PMC 4253621. PMID 25517638.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  18. ^ Kudo, Yotaro; Tateishi, Keisuke; Yamamoto, Keisuke; Yamamoto, Shinzo; Asaoka, Yoshinari; Ijichi, Hideaki; Nagae, Genta; Yoshida, Haruhiko; Aburatani, Hiroyuki (2012-04-01). "Loss of 5-hydroxymethylcytosine is accompanied with malignant cellular transformation". Cancer Science. 103 (4): 670–676. doi:10.1111/j.1349-7006.2012.02213.x. ISSN 1349-7006.
  19. ^ Wu, Bo-Kuan; Brenner, Charles (2014-12-11). "Suppression of TET1-Dependent DNA Demethylation is Essential for KRAS-Mediated Transformation". Cell reports. 9 (5): 1827–1840. doi:10.1016/j.celrep.2014.10.063. ISSN 2211-1247. PMC 4268240. PMID 25466250.

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