Display options
Cite
Meng Q, Sun X, Wang J, et al. The important application of thioridazine in the endometrial cancer. Am J Transl Res. 2016;8(6):2767-75
Meng, Q., Sun, X., Wang, J., Wang, Y., & Wang, L. (2016). The important application of thioridazine in the endometrial cancer. American journal of translational research, 8(6), 2767-75.
Meng, Qiong, et al. "The important application of thioridazine in the endometrial cancer." American journal of translational research vol. 8,6 (2016): 2767-75.
Meng Q, Sun X, Wang J, Wang Y, Wang L. The important application of thioridazine in the endometrial cancer. Am J Transl Res. 2016 Jun 15;8(6):2767-75. eCollection 2016. PMID: 27398159; PMCID: PMC4931170.
Copy Download .nbib Format: NLM
Share it on

Am J Transl Res. 2016 Jun 15;8(6):2767-75. eCollection 2016.

The important application of thioridazine in the endometrial cancer.

American journal of translational research

Qiong Meng, Xiao Sun, Jing Wang, Yudong Wang, Lihua Wang

Affiliations

  1. Department of Anesthesiology, International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University Shanghai, China.
  2. Laboratory for Gynecologic Oncology, International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University Shanghai, China.
  3. Department of Gynecology, International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University Shanghai, China.

PMID: 27398159 PMCID: PMC4931170

Abstract

BACKGROUND: Endometrial cancer (ECa) is one of the serious healthy burden for female worldwide. The treatments of ECa focus on the application of endocrine therapy and aberrant signaling proteins expression recently years. Medroxyprogesterone acrtate (MPA) plays crucial role in the endocrine therapy for ECa patients. However, the outcomes are still not ideal in the advanced stage tumor, especially in the progesterone-resistant ECa. Thioridazine (THIO) is an anti-psychotic agent, which has been reported to suppress the development of several human cancers. In this study, we aimed at to explore the clinical significant of THIO in the treatment of ECa.

METHODS: Two ECa cell lines (ISK and KLE) were enrolled in this study, and were grouped into fore groups based on the treatment with different agents. Methylthiazolyldiphenyl-tetrazolium bromide (MTT) assay was used to analyze the viability of ECa cell lines. The apoptosis of ECa cells was examined by using the flow cytometer. To investigate the expression of important proteins, we applied the quantitative real-time RT-PCR (qRT-PCR) method and western blot analysis.

RESULTS: The viability of ECa cells was downregulated, and the apoptosis of ECa cells was upregulated after treating with the THIO plus MPA. The expression of progesterone receptor B (PRB) and dopamine receptor D2 (DRD2) were increased, and epidermal growth factor receptor (EGFR) and p-AKT were decreased in the THIO+MPA group. All these results suggested that the THIO could promote MPA to inhibit the growth of cells in ECa, especially in the progesterone-resistant ECa.

CONCLUSION: Taken together, all the data in the present study suggested that the THIO plus MPA might act as the suppressor of tumor growth in ECa by inhibiting the PI3K/AKT signal transduction pathway, which was mediated by PRB, DRD2 and EGFR.

Keywords: MPA; Thioridazine; endometrial cancer

References

  1. Oncol Rep. 2015 Feb;33(2):799-809 - PubMed
  2. J Obstet Gynaecol Res. 2015 Oct;41(10 ):1653-60 - PubMed
  3. Oncol Lett. 2015 Dec;10(6):3457-3465 - PubMed
  4. Oncogene. 2004 Jul 29;23 (34):5853-7 - PubMed
  5. Gynecol Oncol. 2007 Apr;105(1):45-54 - PubMed
  6. Cancer. 1995 Jan 1;75(1 Suppl):270-94 - PubMed
  7. J Reprod Med. 2014 Mar-Apr;59(3-4):113-20 - PubMed
  8. Int J Physiol Pathophysiol Pharmacol. 2013 May 27;5(2):109-19 - PubMed
  9. Semin Oncol. 2009 Apr;36(2):145-54 - PubMed
  10. Hematol Oncol Clin North Am. 2002 Jun;16(3):579-88, viii - PubMed
  11. J Cancer Res Ther. 2015 Apr-Jun;11(2):345-51 - PubMed
  12. EMBO J. 2000 Jul 3;19(13):3159-67 - PubMed
  13. Cancer. 2010 Aug 1;116(15):3603-13 - PubMed
  14. Cell. 2012 Jun 8;149(6):1284-97 - PubMed
  15. Steroids. 2003 Nov;68(10-13):795-800 - PubMed
  16. J Clin Endocrinol Metab. 2004 Mar;89(3):1429-42 - PubMed
  17. J Cancer Prev. 2015 Dec;20(4):268-74 - PubMed
  18. Biochem Res Int. 2012;2012:738274 - PubMed
  19. Proc Natl Acad Sci U S A. 1999 Apr 13;96(8):4240-5 - PubMed
  20. Cancer Res. 2006 Mar 15;66(6):3126-36 - PubMed
  21. Palliat Med. 2002 Jul;16(4):279-84 - PubMed
  22. Oncol Lett. 2015 Sep;10(3):1902-1906 - PubMed
  23. J Cell Biochem Suppl. 1995;23:160-4 - PubMed
  24. Br J Cancer. 2009 Jan 13;100(1):89-95 - PubMed
  25. Cochrane Database Syst Rev. 2014 May 15;(5):CD010681 - PubMed
  26. N Engl J Med. 1996 Aug 29;335(9):640-9 - PubMed
  27. Eur J Gynaecol Oncol. 2008;29(1):19-25 - PubMed
  28. CA Cancer J Clin. 2011 Mar-Apr;61(2):69-90 - PubMed
  29. Oncogene. 2003 Dec 8;22(56):8983-98 - PubMed
  30. Nanotoxicology. 2016 Aug;10(6):680-8 - PubMed
  31. Int J Radiat Oncol Biol Phys. 2004;59(2 Suppl):21-6 - PubMed
  32. CA Cancer J Clin. 2011 Jul-Aug;61(4):212-36 - PubMed
  33. Hum Pathol. 1995 Nov;26(11):1268-74 - PubMed
  34. Oncotarget. 2014 Jul 15;5(13):4929-34 - PubMed
  35. BMJ. 2011 Jul 06;343:d3954 - PubMed
  36. Apoptosis. 2012 Sep;17(9):989-97 - PubMed
  37. Curr Opin Endocrinol Diabetes Obes. 2015 Dec;22(6):495-501 - PubMed

Publication Types