Distribution of SET/I2PP2A protein in gastrointestinal tissues


Autoři: Koji Umata aff001;  Yusuke Sakai aff002;  Shunta Ikeda aff001;  Shunya Tsuji aff001;  Hideyoshi Kawasaki aff001;  Takashi Ohama aff001;  Koichi Sato aff001
Působiště autorů: Laboratory of Veterinary Pharmacology, Joint Faculty of Veterinary Medicine, Yamaguchi University, Yamaguchi, Japan aff001;  Laboratory of Veterinary Pathology, Joint Faculty of Veterinary Medicine, Yamaguchi University, Yamaguchi, Japan aff002
Vyšlo v časopise: PLoS ONE 14(9)
Kategorie: Research Article
doi: 10.1371/journal.pone.0222845

Souhrn

SET (also called I2PP2A and TIF-1) is a multi-functional protein that regulates a variety of cell signaling including nucleosome assembly, histone binding, and tumorigenesis. Elevated SET protein levels are observed in various human tumors, and are correlated with poor prognosis and drug-resistance. We recently reported that SET protein levels in cancer cells were positively correlated with poor prognosis of gastric cancer patients. Using immunohistochemistry, SET protein was observed not only in cancer cells, but also in some interstitial cells. However, the tissue distribution of SET has not been investigated. Here we performed co-immunofluorescent staining to characterize SET protein distribution in gastrointestinal tissues. We found that even though the positive rate is much lower than epithelial cells, SET protein is also expressed in non-epithelial cells, such as monocytes/macrophages, neural cells, myofibroblasts, and smooth muscle cells. Our results indicate an extensive role of SET in a variety of cell types.

Klíčová slova:

Epithelial cells – Gastrointestinal tract – Immunohistochemistry techniques – Immunofluorescence staining – Smooth muscle cells – Gastrointestinal analysis – Duodenum – Tissue distribution


Zdroje

1. von Lindern M, van Baal S, Wiegant J, Raap A, Hagemeijer A, Grosveld G. Can, a putative oncogene associated with myeloid leukemogenesis, may be activated by fusion of its 3’ half to different genes: characterization of the set gene. Mol Cell Biol. 1992;12: 3346–3355. doi: 10.1128/mcb.12.8.3346 1630450

2. Matsumoto K, Nagata K, Ui M, Hanaoka F. Template activating factor I, a novel host factor required to stimulate the adenovirus core DNA replication. J Biol Chem. 1993;268: 10582–10587. 8486711

3. Li M, Guo H, Damuni Z. Purification and characterization of two potent heat-stable protein inhibitors of protein phosphatase 2A from bovine kidney. Biochemistry. 1995;34: 1988–1996. doi: 10.1021/bi00006a020 7531497

4. Li M, Makkinje A, Damuni Z. The myeloid leukemia-associated protein SET is a potent inhibitor of protein phosphatase 2A. J Biol Chem. 1996;271: 11059–11062. doi: 10.1074/jbc.271.19.11059 8626647

5. Nagata K, Kawase H, Handa H, Yano K, Yamasaki M, Ishimi Y, et al. Replication factor encoded by a putative oncogene, set, associated with myeloid leukemogenesis. Proc Natl Acad Sci USA. 1995;92: 4279–4283. doi: 10.1073/pnas.92.10.4279 7753797

6. Saito S, Miyaji-Yamaguchi M, Shimoyama T, Nagata K. Functional domains of template-activating factor-I as a protein phosphatase 2A inhibitor. Biochem Biophys Res Commun. 1999;259: 471–475. doi: 10.1006/bbrc.1999.0790 10362532

7. Kawase H, Okuwaki M, Miyaji M, Ohba R, Handa H, Ishimi Y, et al. NAP-I is a functional homologue of TAF-I that is required for replication and transcription of the adenovirus genome in a chromatin-like structure. Genes Cells. 1996;1: 1045–1056. 9077453

8. Wang D, Kon N, Lasso G, Jiang L, Leng W, Zhu WG, et al. Acetylation-regulated interaction between p53 and SET reveals a widespread regulatory mode. Nature. 2016;538: 118–122. doi: 10.1038/nature19759 27626385

9. Fan Z, Beresford PJ, Oh DY, Zhang D, Lieberman J. Tumor suppressor NM23-H1 is a granzyme A-activated DNase during CTL-mediated apoptosis, and the nucleosome assembly protein SET is its inhibitor. Cell. 2003;112: 659–672. doi: 10.1016/s0092-8674(03)00150-8 12628186

10. Seo SB, McNamara P, Heo S, Turner A, Lane WS, Chakravarti D. Regulation of histone acetylation and transcription by INHAT, a human cellular complex containing the set oncoprotein. Cell. 2001;104: 119–130. doi: 10.1016/s0092-8674(01)00196-9 11163245

11. Liu H, Gu Y, Wang H, Yin J, Zheng G, Zhang Z, et al. Overexpression of PP2A inhibitor SET oncoprotein is associated with tumor progression and poor prognosis in human non-small cell lung cancer. Oncotarget. 2015;6: 14913–14925. doi: 10.18632/oncotarget.3818 25945834

12. Cristóbal I, Rincón R, Manso R, Caramés C, Zazo S, Madoz-Gúrpide J, et al. Deregulation of the PP2A inhibitor SET shows promising therapeutic implications and determines poor clinical outcome in patients with metastatic colorectal cancer. Clin Cancer Res. 2015;21: 347–356. doi: 10.1158/1078-0432.CCR-14-0724 25388166

13. Janghorban M, Farrell AS, Allen-Petersen BL, Pelz C, Daniel CJ, Oddo J, et al. Targeting c-MYC by antagonizing PP2A inhibitors in breast cancer. Proc Natl Acad Sci USA. 2014;111: 9157–9162. doi: 10.1073/pnas.1317630111 24927563

14. Farrell AS, Allen-Petersen B, Daniel CJ, Wang X, Wang Z, Rodriguez S, et al. Targeting inhibitors of the tumor suppressor PP2A for the treatment of pancreatic cancer. Mol Cancer Res. 2014;12: 924–939. doi: 10.1158/1541-7786.MCR-13-0542 24667985

15. Enjoji S, Yabe R, Tsuji S, Yoshimura K, Kawasaki H, Sakurai M, et al. Stemness Is Enhanced in Gastric Cancer by a SET/PP2A/E2F1 Axis. Mol Cancer Res. 2018;16: 554–563. doi: 10.1158/1541-7786.MCR-17-0393 29330298

16. Cristóbal I, Garcia-Orti L, Cirauqui C, Cortes-Lavaud X, García-Sánchez MA, Calasanz MJ, et al. Overexpression of SET is a recurrent event associated with poor outcome and contributes to protein phosphatase 2A inhibition in acute myeloid leukemia. Haematologica. 2012;97: 543–550. doi: 10.3324/haematol.2011.050542 22133779

17. Enjoji S, Yabe R, Fujiwara N, Tsuji S, Vitek MP, Mizuno T, et al. The therapeutic effects of SET/I2PP2A inhibitors on canine melanoma. J Vet Med Sci. 2015; doi: 10.1292/jvms.15-0193 26062569

18. Christensen DJ, Chen Y, Oddo J, Matta KM, Neil J, Davis ED, et al. SET oncoprotein overexpression in B-cell chronic lymphocytic leukemia and non-Hodgkin lymphoma: a predictor of aggressive disease and a new treatment target. Blood. 2011;118: 4150–4158. doi: 10.1182/blood-2011-04-351072 21844565

19. Bhutia YD, Hung SW, Krentz M, Patel D, Lovin D, Manoharan R, et al. Differential processing of let-7a precursors influences RRM2 expression and chemosensitivity in pancreatic cancer: role of LIN-28 and SET oncoprotein. PLoS ONE. 2013;8: e53436. doi: 10.1371/journal.pone.0053436 23335963

20. ten Klooster JP, Leeuwen I v, Scheres N, Anthony EC, Hordijk PL. Rac1-induced cell migration requires membrane recruitment of the nuclear oncogene SET. EMBO J. 2007;26: 336–345. doi: 10.1038/sj.emboj.7601518 17245428

21. Neviani P, Santhanam R, Trotta R, Notari M, Blaser BW, Liu S, et al. The tumor suppressor PP2A is functionally inactivated in blast crisis CML through the inhibitory activity of the BCR/ABL-regulated SET protein. Cancer Cell. 2005;8: 355–368. doi: 10.1016/j.ccr.2005.10.015 16286244

22. Trotta R, Ciarlariello D, Dal Col J, Mao H, Chen L, Briercheck E, et al. The PP2A inhibitor SET regulates granzyme B expression in human natural killer cells. Blood. 2011;117: 2378–2384. doi: 10.1182/blood-2010-05-285130 21156847

23. Arif M, Wei J, Zhang Q, Liu F, Basurto-Islas G, Grundke-Iqbal I, et al. Cytoplasmic retention of protein phosphatase 2A inhibitor 2 (I2PP2A) induces Alzheimer-like abnormal hyperphosphorylation of Tau. J Biol Chem. 2014;289: 27677–27691. doi: 10.1074/jbc.M114.565358 25128526

24. Trakhtenberg EF, Wang Y, Morkin MI, Fernandez SG, Mlacker GM, Shechter JM, et al. Regulating Set-β’s Subcellular Localization Toggles Its Function between Inhibiting and Promoting Axon Growth and Regeneration. J Neurosci. 2014;34: 7361–7374. doi: 10.1523/JNEUROSCI.3658-13.2014 24849368

25. Tanimukai H, Grundke-Iqbal I, Iqbal K. Up-regulation of inhibitors of protein phosphatase-2A in Alzheimer’s disease. Am J Pathol. 2005;166: 1761–1771. doi: 10.1016/S0002-9440(10)62486-8 15920161

26. Wang X, Blanchard J, Grundke-Iqbal I, Wegiel J, Deng H-X, Siddique T, et al. Alzheimer disease and amyotrophic lateral sclerosis: an etiopathogenic connection. Acta Neuropathol. 2014;127: 243–256. doi: 10.1007/s00401-013-1175-9 24136402


Článek vyšel v časopise

PLOS One


2019 Číslo 9

Nejčtenější v tomto čísle

Tomuto tématu se dále věnují…


Kurzy

Zvyšte si kvalifikaci online z pohodlí domova

Léčba bolesti v ordinaci praktického lékaře
nový kurz
Autoři: MUDr. PhDr. Zdeňka Nováková, Ph.D.

Revmatoidní artritida: včas a k cíli
Autoři: MUDr. Heřman Mann

Jistoty a nástrahy antikoagulační léčby aneb kardiolog - neurolog - farmakolog - nefrolog - právník diskutují
Autoři: doc. MUDr. Štěpán Havránek, Ph.D., prof. MUDr. Roman Herzig, Ph.D., doc. MUDr. Karel Urbánek, Ph.D., prim. MUDr. Jan Vachek, MUDr. et Mgr. Jolana Těšínová, Ph.D.

Léčba akutní pooperační bolesti
Autoři: doc. MUDr. Jiří Málek, CSc.

Nové antipsychotikum kariprazin v léčbě schizofrenie
Autoři: prof. MUDr. Cyril Höschl, DrSc., FRCPsych.

Všechny kurzy
Kurzy Doporučená témata Časopisy
Přihlášení
Zapomenuté heslo

Nemáte účet?  Registrujte se

Zapomenuté heslo

Zadejte e-mailovou adresu se kterou jste vytvářel(a) účet, budou Vám na ni zaslány informace k nastavení nového hesla.

Přihlášení

Nemáte účet?  Registrujte se