DYNAMICS OF CONCENTRATIONS OF NO-SYSTEM COMPONENTS DURING B16/F10 MELANOMA GROWTH IN FEMALE MICE WITH CHRONIC NEUROGENIC PAIN
PDF (Русский)

Keywords

МЕЛАНОМА B16/F10
NO-СИСТЕМА
B16/F10 MELANOMA
CHRONIC NEUROGENIC PAIN
SKIN
TUMOR
MICE
NO-SYSTEM

How to Cite

Kit, O., Frantsiyants, Y., Kotieva, I., Surikova, Y., Kaplieva, I., Bandovkina, V., Trepitaki, L., Pogorelova, Y., & Sidorenko, Y. (2019). DYNAMICS OF CONCENTRATIONS OF NO-SYSTEM COMPONENTS DURING B16/F10 MELANOMA GROWTH IN FEMALE MICE WITH CHRONIC NEUROGENIC PAIN. Voprosy Onkologii, 65(6), 898–903. https://doi.org/10.37469/0507-3758-2019-65-6-898-903

Abstract

Since chronic neurogenic pain has been reported to affect biological characteristics of B16/F10 melanoma, the purpose of the study was to analyze concentrations of components of the NO-system in mice during the growth of transplantable B16/F10 melanoma combined with chronic neurogenic pain.

Methods. The study included 64 female mice. Melanoma was transplanted under the skin of the back to animals of the main group 2 weeks after the bilateral sciatic nerve ligation. Levels of NOS-3, NOS-2, endothelin-1, L-arginine, citrulline, total nitrite and ADMA were determined by ELISA in the intact skin and in tumor tissues.

Results. The study showed that the dynamics of the studied parameters differed in tumor growth alone and in combination with chronic pain. Stably increased levels of NO-synthases in the tumor and stably increased ADMA levels with their decrease by week 3 of the growth were registered in the tumor growth with pain.

Conclusions. Chronic pain probably contributes to the development of immunological tolerance to tumor antigens in the skin. Conditions are formed that facilitate the survival of tumor cells and contribute to the further development of melanoma. The dynamics of the NO-system activity can stimulate neoangiogenesis and enhance tumor invasion. Changes in the ADMA inhibitor levels in the tumor growth combined with chronic pain may indicate the control of NO levels through the metabolic regulation of NO-synthase activity, thus providing increased melanoma invasiveness.

https://doi.org/10.37469/0507-3758-2019-65-6-898-903
PDF (Русский)

References

Choudhari S.K., Chaudhary M., Bagde S., Gadbail A.R., Joshi V. Nitric oxide and cancer: a review. World J Surg Oncol. 2013;11:118. DOI: 10.1186/1477-7819-11-118

Rizi B.S., Achreja A., Nagrath D. Nitric oxide - the forgotten child of tumor metabolism. Trends Cancer. 2017;3(9):659-672. DOI: 10.1016/j.trecan.2017.07.005

De Alba J., Clayton N.M., Collins S.D., Colthup P., Chessell I., Knowles R.G. GW274150, a novel and highly selective inhibitor of the inducible isoform of nitric oxide synthase (iNOS), shows analgesic effects in rat models of inflammatory and neuropathic pain. pain. 2006;120:170-181.

Naik A.K., Tandan S.K., Kumar D., Dudhgaonkar S.P. Nitric oxide and its modulators in chronic constriction injury-induced neuropathic pain in rats. Eur J Pharmacol. 2006;530:59-69.

Kuboyama K, Tsuda M, Tsutsui M, Toyohara Y, Tozaki-Saitoh H, Shimokawa H, Yanagihara N, Inoue K. Reduced spinal microglial activation and neuropathic pain after nerve injury in mice lacking all three nitric oxide synthases. Mol Pain. 2011;7:50. DOI: 10.1186/1744-8069-7-50

Yang X Zhang J, Liu X Zheng Y Bo J, Zhou X, Wang J, Ma Z. Role of nitric oxide synthase in the development of bone cancer pain and effect of L-NMMA. Mol Med Rep. 2016;13(2):1220-6. 10.3892/ mmr.2015.4647. DOI: 10.3892/mmr.2015.4647

Worldwide palliative care alliance (WPCA); World Health Organization 2015.- www.who.int/nmh/Global_Atlas_of_ Palliative_Care.pdf.

Каприн А.Д., Абузарова Г.Р., Хороненко В.Э. и др. Фармакотерапия хронического болевого синдрома у онкологических пациентов. - М.: МНИОИ им. П.А. Герцена - филиал ФГБУ "ФМИЦ им. П.А. Герцена" Минздрава России. 2015. 48 с.

Яхно H.H., Кукушкин М.Л., Давыдов О.С. и др. Результаты российского эпидемиологического исследования распространенности нейропатической боли, ее причин и характеристик в популяции амбулаторных больных, обратившихся к врачу неврологу. Журнал Боль. 2008;20(3):24-32.

Решетняк Д.В., Смирнова В.С., Кукушкин М.Л. Половые различия при изменении биохимических показателей крови у крыс в ответ на острую соматическую и хроническую нейрогенную боль. Журнал Боль. 2004;2(3):12-16.

Кит О.И., Франциянц Е.М., Котиева И.М. и др. Некоторые механизмы повышения злокачественности меланомы на фоне хронической боли у самок мышей. Российский журнал боли. 2017;2(53):14-20.

Кит О.И., Котиева И.М., Франциянц Е.М. и др. Влияние хронической нейропатической боли на течение злокачественного процесса меланомы В16/F10 у самцов мышей. Известия высших учебных заведений. Северо-Кавказский регион. Серия: Естественные науки. 2019;1(201):106-111.

Кит О. И., Котиева И.М., Франциянц Е.М. и др. Регуляция ангиогенеза факторами роста в интактной и патологически измененной коже самок мышей при злокачественной меланоме, развивающейся на фоне хронической боли. Российский журнал боли. 2017;3-4(54):17-25.

Mazzoni, A., Bronte, V., Visintin, A., Spitzer, J.H., Apolloni, E., Serafini, P., Zanovello, P., Segal, D.M. Myeloid suppressor lines inhibit T-cell responses by an NO-dependent mechanism. J. Immunol. 2002;168:689-695.

Viola A., Bronte V. Metabolic mechanisms of cancer-induced inhibition of immune responses. Semin Cancer Biol. 2007;17(4):309-316.

Ziche M., Morbidelli L. Molecular regulation of tumour angiogenesis by nitric oxide. European Cytokine Network. 2009;20(4):164-170. DOI: 10.1684/ecn.2009.0169

Saleh A, Stathopoulou MG, Dadé S, Ndiaye NC, Azimi-Nezhad M, Murray H, Masson C, Lamont J, Fitzgerald P, Visvikis-Siest S. Angiogenesis related genes NOS3, CD14, MMP3 and IL4R are associated to VEGF gene expression and circulating levels in healthy adults. BMC Med Genet. 2015;16:90. DOI: 10.1186/s12881-015-0234-6

Tu YT, Tao J, Liu YQ, Li Y, Huang CZ, Zhang XB, Lin Y Expression of endothelial nitric oxide synthase and vascular endothelial growth factor in human malignant melanoma and their relation to angiogenesis. Clin Exp Dermatol. 2006;31(3):413-8. DOI: 10.1111/j.1365-2230.2006.02123.x

Barbieri A., Palma G., Rosati A., Giudice A., Falco A., Petrillo A., Mario Petrillo, Bimonte S., Benedetto M. Di, Esposito G., Stiuso P, Abbruzzese A., Caraglia M., Arra C. Role of endothelial nitric oxide synthase (eNOS) in chronic stress-promoted tumour growth. J. Cell. Mol. Med. 2012;16(4):920-926. DOI: 10.111Vj.1582-4934.2011.01375.x.

Lankhorst S., Kappers MH, van Esch JH, Danser AH, van den Meiracker AH. Hypertension during vascular endothelial growth factor inhibition: focus on nitric oxide, endothelin-1, and oxidative stress. Antioxid Redox Signal.2014;20(1):135-45. DOI: 10.1089/ars.2013.5244

Vahora H., Khan M.A., Alalami U., Hussain A. The Potential Role of Nitric Oxide in Halting Cancer Progression Through Chemoprevention. J Cancer Prev. 4010;21(1):1-12. DOI: 10.15430/JCP.2016.21.1.1

Lahdenranta J, Hagendoorn J, Padera TP, Hoshida T, Nelson G, Kashiwagi S. Endothelial nitric oxide synthase mediates lymphangiogenesis and lymphatic metastasis. Cancer Res. 2009;69:2801-2808.

Kashiwagi S, Izumi X Gohongi T, Demou ZN, Xu L, Huang PL, Buerk DG, Munn LL, Jain RK, Fukumura D. NO mediates mural cell recruitment and vessel morphogenesis in murine melanomas and tissue-engineered blood vessels. J Clin Invest. 2005;115(7):1816-27.

Creative Commons License

This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

© АННМО «Вопросы онкологии», Copyright (c) 2019