Expression of TRA2B in endometrial carcinoma and its regulatory roles in endometrial carcinoma cells.

Dhruba Paudel, Yiqin Ouyang, Qingting Huang, Wei Zhou, Jianjun Wang, Maxwell Enayat Poorekhorsandi, Bipin Dhakal, Xiaowen Tong
Author Information
  1. Dhruba Paudel: Department of Gynecology and Obstetrics, Tongji Hospital Affiliated to Tongji University, Shanghai 200065, P.R. China.
  2. Yiqin Ouyang: Department of Gynecology and Obstetrics, Tongji Hospital Affiliated to Tongji University, Shanghai 200065, P.R. China.
  3. Qingting Huang: Department of Gynecology and Obstetrics, Tongji Hospital Affiliated to Tongji University, Shanghai 200065, P.R. China.
  4. Wei Zhou: Department of Gynecology and Obstetrics, Tongji Hospital Affiliated to Tongji University, Shanghai 200065, P.R. China.
  5. Jianjun Wang: Department of Gynecology and Obstetrics, Tongji Hospital Affiliated to Tongji University, Shanghai 200065, P.R. China.
  6. Maxwell Enayat Poorekhorsandi: Department of Gynecology and Obstetrics, Tongji Hospital Affiliated to Tongji University, Shanghai 200065, P.R. China.
  7. Bipin Dhakal: Department of Gynecology and Obstetrics, Tongji Hospital Affiliated to Tongji University, Shanghai 200065, P.R. China.
  8. Xiaowen Tong: Department of Gynecology and Obstetrics, Tongji Hospital Affiliated to Tongji University, Shanghai 200065, P.R. China.

Abstract

Expression levels of Transformer 2 protein homolog beta (TRA2B) in patients with endometrial carcinoma were assessed to investigate the impact of TRA2B on endometrial carcinoma cells. Furthermore, we analyzed the expression of several genes in the tissue samples from patients with endometrial cancer (EC) to identify whether cancer related genes we chose are differently expressed between the endometrial carcinoma tissues and adjacent normal tissues. The results of RT-qPCR analysis, western blot technology and immunofluorescence method consistently manifested that the expression of several genes in endometrial carcinoma tissue was significantly dysregulated between the two groups. Among the dysregulated genes, the strongly upregulated TRA2B in the tissues and serum from patients with EC was selected for further analysis. Endometrial carcinoma cells were transfected with chemically synthesized TRA2B plasmid, siRNA-TRA2B and their corresponding negative control respectively to assess the effects of TRA2B on the EC cells. Overexpression of TRA2B increased both the cell viability and proliferation potency of EC cells. Whereas, the viability and the proliferation ability of EC cells were strongly decreased by siRNA-TRA2B treatment. Furthermore, the invasion of EC cells was promoted by transfection of TRA2B and overexpression of TRA2B decreased the apoptosis of EC cells. Moreover, siRNA-TRA2B transfection inhibited the invasion but accelerated apoptosis of EC cells. Our results demonstrated that TRA2B is closely related to the development of endometrial carcinoma, and inhibition of TRA2B can decrease viability, proliferation and invasion of endometrial carcinoma, suggesting TRA2B is associated with the pathogenesis of human EC. Knockdown of TRA2B may be used for treatment of endometrial carcinoma, furthermore, these findings suggest an experimental foundation to clinical prognostic role of TRA2B in patients with endometrial carcinoma.

Keywords

References

  1. Methods. 2001 Dec;25(4):402-8 [PMID: 11846609]
  2. Hum Mol Genet. 2002 Aug 15;11(17):2037-49 [PMID: 12165565]
  3. Hum Mol Genet. 2004 Mar 1;13(5):509-24 [PMID: 14709600]
  4. Mech Dev. 2004 Jul;121(7-8):991-6 [PMID: 15210204]
  5. Cell Biol Int. 2004;28(11):791-9 [PMID: 15563401]
  6. Cancer Res. 2006 May 1;66(9):4774-80 [PMID: 16651431]
  7. Acta Obstet Gynecol Scand. 2009;88(2):216-21 [PMID: 19037821]
  8. Eur J Obstet Gynecol Reprod Biol. 2009 Apr;143(2):69-74 [PMID: 19195765]
  9. Biochim Biophys Acta. 2010 May-Jun;1799(5-6):448-53 [PMID: 20074680]
  10. Hum Mol Genet. 2010 Jun 1;19(11):2154-67 [PMID: 20190275]
  11. Nat Genet. 2010 Dec;42(12):1077-85 [PMID: 21102462]
  12. Hum Mol Genet. 2011 Jun 15;20(12):2356-65 [PMID: 21447598]
  13. Nucleic Acids Res. 2011 Oct;39(18):8092-104 [PMID: 21724598]
  14. Cell Metab. 2011 Aug 3;14(2):208-18 [PMID: 21803291]
  15. PLoS Genet. 2011 Dec;7(12):e1002390 [PMID: 22194695]
  16. Mol Cell Biol. 2014 Aug;34(15):2857-73 [PMID: 24865968]
  17. Eur J Gynaecol Oncol. 2014;35(6):701-7 [PMID: 25556278]
  18. Oncogenesis. 2016 Apr 04;5:e213 [PMID: 27043659]
  19. Biochem Biophys Res Commun. 2016 Sep 16;478(2):507-12 [PMID: 27381864]
  20. Oncotarget. 2016 Aug 16;7(33):53102-53115 [PMID: 27447978]
  21. Hum Genet. 2017 Sep;136(9):1143-1154 [PMID: 28382513]
  22. Nat Nanotechnol. 2018 Jan;13(1):72-81 [PMID: 29203914]
  23. PLoS One. 2017 Dec 5;12(12):e0189081 [PMID: 29206870]
  24. Oncotarget. 2017 May 30;8(53):91684-91693 [PMID: 29207677]
  25. Gynecol Oncol. 2018 Feb;148(2):383-392 [PMID: 29208367]
  26. Obstet Gynecol. 2018 Jan;131(1):109-116 [PMID: 29215513]
  27. Gynecol Oncol. 2018 Feb;148(2):258-266 [PMID: 29217139]
  28. Am J Obstet Gynecol. 2018 Mar;218(3):329.e1-329.e15 [PMID: 29223598]
  29. J Proteome Res. 2018 Feb 2;17(2):804-812 [PMID: 29235868]
  30. Oncol Lett. 2017 Dec;14(6):7191-7196 [PMID: 29344151]
  31. J Minim Invasive Gynecol. 2018 Sep - Oct;25(6):986-993 [PMID: 29360514]
  32. J Steroid Biochem Mol Biol. 2018 Apr;178:312-321 [PMID: 29360580]
  33. Nat Commun. 2018 Jan 23;9(1):295 [PMID: 29362355]
  34. Gynecol Endocrinol. 2018 Jul;34(7):563-566 [PMID: 29366348]
  35. Cancer Biol Ther. 2018 Mar 4;19(3):160-168 [PMID: 29370558]
  36. Endocr Relat Cancer. 2018 Apr;25(4):381-391 [PMID: 29371332]
  37. Cancer Biol Med. 2017 Nov;14(4):377-386 [PMID: 29372104]
  38. Gen Physiol Biophys. 2017 Dec;36(5):521-529 [PMID: 29372685]
  39. Pathology. 2018 Feb;50(2):238-256 [PMID: 29373116]
  40. Genes (Basel). 2018 Jan 26;9(2):null [PMID: 29373522]
  41. Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2017 Dec;33(12):1628-1634 [PMID: 29382422]
  42. PLoS One. 2018 Jan 31;13(1):e0191793 [PMID: 29385192]
  43. BMC Cancer. 2019 Jan 18;19(1):86 [PMID: 30658617]
  44. J Thromb Haemost. 2019 Aug;17(8):1335-1344 [PMID: 31099477]
  45. J Pathol. 2019 May 18;:null [PMID: 31102277]
  46. Ear Nose Throat J. 1997 Jun;76(6):364 [PMID: 9210800]

Word Cloud

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