Effect of transforming growth factor-β2 on uterine leiomyoma cells proliferation
- Authors: Muratova ND1, Abduvaliev AA2
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Affiliations:
- Tashkent Pediatric Medical Institute, Tashkent, Uzbekistan
- Tashkent Medical Academy, Tashkent, Uzbekistan
- Issue: Vol 96, No 6 (2015)
- Pages: 968-970
- Section: Theoretical and clinical medicine
- Submitted: 28.03.2016
- Published: 15.12.2015
- URL: https://kazanmedjournal.ru/kazanmedj/article/view/1623
- DOI: https://doi.org/10.17750/KMJ2015-968
- ID: 1623
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Full Text
Abstract
Aim. To study the role of transforming growth factor-β2 in the uterine leiomyoma pathogenesis.
Methods. Studies to determine the cytotoxic activity of the transforming growth factor-β2 regarding the temporary cell culture were conducted. The operational material was used from two women of reproductive age with uterine myoma (multiple symptomatic uterine myoma, proliferative type) who underwent hysterectomy. Patients mean age was 43.5±0.57. Obtained temporary culture cells were split into five groups depending on the transforming growth factor-β2 affecting dose (1000, 500, 100, 10 µg/10×106, and culture with no exposure). After incubation living and dead cells were counted at 280 times magnification. The cytotoxic activity was expressed as a percentage of live and dead cells.
Results. Total cell death (necrosis) was 23.0% when using factor at the dose 10 µg/10×106 cells, at the dose 100 µg/ 10×106 cells - 34.5%, at the dose 500 µg/10×106 cells - 44%, at the dose 1000 µg/10×106 cells - 59.5%. The most effective vital life suppressing activity of the transformed cells was observed when exposed to transforming growth factor-β2 at the dose 1000 µg/10×106 cells.
Conclusion. Transforming growth factor-β2 is capable to suppress the proliferating uterine fibroids growth under certain conditions and the dose, it has a significant dose-dependent cytotoxic effect in respect of the neoplasm.
About the authors
N D Muratova
Tashkent Pediatric Medical Institute, Tashkent, Uzbekistan
Author for correspondence.
Email: muratova-84@yandex.ru
A A Abduvaliev
Tashkent Medical Academy, Tashkent, Uzbekistan
Email: muratova-84@yandex.ru
References
- Абдувалиев А.А., Гильдиева М.С. Дифференциальное окрашивание опухолевых клеток трипановым синим для определения апоптоза. Клин. лаб. диагност. 2006: (2): 36-38.
- Абдувалиев А.А., Гильдиева М.С., Татарский В.П. Способ определения индивидуальной лекарственной чувствительности к противоопухолевым препаратам. Клин. лаб. диагност. 2006; (5): 50-52.
- Biswas S., Criswell T., Wang C. Inhibition of transforming growth factor-B signaling in human cancer: targeting a tumor suppressor network as a therapeutic strategy. Clin. Cancer Res. 2006; 12 (14): 4142-4146. http://dx.doi.org/10.1158/1078-0432.CCR-06-0952
- Javelaud D., Mauviel A. Crosstalk mechanisms between the mitogen-activated protein kinase pathways and Smad signaling downstream of TGF-beta: implications for carcinogenesis. Oncogene. 2005; 24: 5742-5750. http://dx.doi.org/10.1038/sj.onc.1208928
- Kajdaniuk D., Marek B., Borgiel-Marek H., Kos-Kudła B. Transforming growth factor β1 (TGFβ1) in physiology and pathology. Endokrynol. Pol. 2013; 64 (5): 384-396. http://dx.doi.org/10.5603/EP.2013.0022
- Kaminska B., Kocyk M., Kijewska M. TGF beta signaling and its role in glioma pathogenesis. Adv. Exp. Med. Biol. 2013; 986: 171-187. http://dx.doi.org/10.1007/978-94-007-4719-7_9
- Minhajat R., Mori D., Yamasaki F. Organ-specific endoglin (CD105) expression in the angiogenesis of human cancers. Pathol. Int. 2006; 56: 717-723. http://dx.doi.org/10.1111/j.1440-1827.2006.02037.x
- Prud’homme G.J., Glinka Y. Neuropilins are multifunctional coreceptors involved in tumor initiation, growth, metastasis and immunity. Oncotarget. 2012; 3 (9): 921-939. http://dx.doi.org/10.18632/oncotarget.626
- Ribatti D. Mast cells and macrophages exert beneficial and detrimental effects on tumor progression and angiogenesis. Immunol. Lett. 2013; 152 (2): 83-88. http://dx.doi.org/10.1016/j.imlet.2013.05.003
- Samarakoon R., Overstreet J.M., Higgins P.J. TGF-β signaling in tissue fibrosis: redox controls, target genes and therapeutic opportunities. Cell Signal. 2013; 25 (1): 264-268. http://dx.doi.org/10.1016/j.cellsig.2012.10.003
- Santos J.I., Teixeira A.L., Dias F. et al. Restoring TGFβ1 pathway-related microRNAs: possible impact in metastatic prostate cancer development. Tumour. Biol. 2014; 35 (7): 6245-6253. http://dx.doi.org/10.1007/s13277-014-1887-z
- Zeglinski M.R., Hnatowich M., Jassal D.S., Dixon I.M. SnoN as a novel negative regulator of TGF-β/Smad signaling: a target for tailoring organ fibrosis. Am. J. Physiol. Heart Circ. Physiol. 2015; 308 (2): H75-H82. http://dx.doi.org/10.1152/ajpheart.00453.2014