oncotomskСибирский онкологический журналSiberian journal of oncology1814-48612312-3168Tomsk National Research Medical Сепtеr of the Russian Academy of Sciences10.21294/1814-4861-2026-25-1-74-84oncotomsk-4111Research ArticleЛАБОРАТОРНЫЕ И ЭКСПЕРИМЕНТАЛЬНЫЕ ИССЛЕДОВАНИЯLABORATORY AND EXPERIMENTAL STUDIESСтволовые клетки колоректального рака в первичной опухолиCancer stem cells in colorectal cancerhttps://orcid.org/0009-0008-2228-3351КрюковаВ. В.KryukovaV. V.

Крюкова Виктория Викторовна, кандидат медицинских наук, доцент кафедры госпитальной хирургии с курсом детской хирургии 

672000, г. Чита, ул. Горького, 39а

Victoria V. Kryukova, MD, PhD, Associate Professor, Department of Hospital Surgery with a Course in Pediatric Surgery 

39a, Gorky St., Chita, 672000

https://orcid.org/0000-0002-2166-5154ЦепелевВ. Л.TsepelevV. L.

Цепелев Виктор Львович, доктор медицинских наук, профессор, заведующий кафедрой госпитальной хирургии с курсом детской хирургии 

Author ID (Scopus): 55548678900.

672000, г. Чита, ул. Горького, 39а

Viktor L. Tsepelev, MD, DSc, Professor, Head of the Department of Hospital Surgery with a Course in Pediatric Surgery 

Author ID (Scopus): 55548678900.

39a, Gorky St., Chita, 672000

viktorcepelev@mail.ruhttps://orcid.org/0000-0002-8601-3499ТерешковП. П.TereshkovP. P.

Терешков Павел Петрович, кандидат медицинских наук, заведующий лабораторией экспериментальной и клинической биохимии и иммунологии НИИ молекулярной медицины 

Author ID (Scopus): 8583303300.

672000, г. Чита, ул. Горького, 39а

Pavel P. Tereshkov, MD, PhD, Head of the Laboratory of Experimental and Clinical Biochemistry and Immunology, Research Institute of Molecular Medicine 

Author ID (Scopus): 8583303300.

39a, Gorky St., Chita, 672000

ФГБОУ ВО «Читинская государственная медицинская академия» Минздрава РоссииРоссияChita State Medical Academy, Ministry of Health of RussiaRussian Federation2026070420262517484Copyright © Крюкова В.В., Цепелев В.Л., Терешков П.П., 20262026Крюкова В.В., Цепелев В.Л., Терешков П.П.Kryukova V.V., Tsepelev V.L., Tereshkov P.P.This work is licensed under a Creative Commons Attribution 4.0 License.https://www.siboncoj.ru/jour/article/view/4111

Актуальность. Раковые стволовые клетки (РСК) являются одной из причин прогрессирования и рецидивов колоректального рака (КРР). Детальное изучение фенотипа данных клеток, их иммунобиологических свойств необходимо для разработки методов лечения КРР. Цель исследования – определить содержание РСК, имеющих фенотип EpCAMhighCD44+, в первичной опухоли у больных КРР, а также экспрессию на их поверхности CD133, CD166, CD24 и CD184. Материал и методы. Выполнено одномоментное поперечное исследование клеточного состава опухолевой ткани 123 больных аденокарциномой толстой кишки III cтадии. Контрольную группу составили 87 больных, оперированных по поводу неопухолевых заболеваний толстой кишки. Для получения суспензии клеток опухолевой ткани использовали ферментативный метод. Гейтирование клеток нелимфоидного происхождения (CD45- ) производили в зависимости от экспрессии на их поверхности молекулы адгезии эпителиальных клеток EpCAM и дифференцировочного антигена CD44. Экспрессия EpCAM, CD44, СD133, CD166, СD184 и CD24 на РСК исследована методом проточной цитометрии. Результаты. Относительное содержание РСК с фенотипом CD45- EpCAMhighCD44+ в опухолевой ткани при КРР составило 17,15 [11,76; 26,44] % от пула клеток нелимфоидного происхождения. У больных КРР в структуре РСК обнаружено 42,83 [37,07; 51,77] % клеток, одновременно экспрессирующих СD133 и CD166, и 57,17 [48,23; 62,93] % клеток, экспрессирующих дифференцировочный антиген CD133. Все РСК в первичной опухоли экспрессируют CD184, и 95,18 [88,48; 97,98] % из них одновременно экспрессируют CD24. При высокодифференцированной аденокарциноме количество клеток EpCAMhighCD44+ в первичной опухоли в 1,5 раза ниже по отношению к умеренно дифференцированному КРР (U=326,5, p=0,002) и в 2,1 раза (U=21,0, p<0,001) – по сравнению с низкодифференцированной аденокарциномой. У пациентов c КРР IIIС стадии на 13 % увеличивается количество опухолевых клеток с фенотипом EpCAMhighCD44+CD133+CD166+ по отношению к больным КРР IIIВ стадии (U=1116,0, p=0,007). Заключение. В первичной опухоли при КРР раковые стволовые клетки, высокоэкспрессирующие молекулу адгезии эпителиальных клеток EpCAM и CD44, составляют 17,2 % от пула клеток нелимфоидного происхождения. Количество опухолевых клеток EpCAMhighCD44+ увеличивается при снижении степени дифференцировки аденокарциномы.

Background. Cancer stem cells (CSCs) are considered to be responsible for progression and recurrence of colorectal cancer (CRC). A detailed study of the phenotype of these cells and their immunobiological properties is necessary for developing CRC treatments. The aim of the study was to assess the percentage of EpCAMhigh/CD44+ cancer stem cells in colorectal cancer and to detect the expression of CD133, CD166, CD24 and CD184 on their surface. Material and Methods. A one-stage cross-sectional study of the cellular composition of tumor tissue was performed in 123 patients with stage III colon adenocarcinoma. The control group consisted of 87 patients who underwent surgery for non-neoplastic diseases of the colon. An enzymatic method was used to obtain a suspension of tumor tissue cells. Gating of non-lymphoid cells (CD45-) was performed depending on the expression of the epithelial cell adhesion molecule EpCAM and the differentiation antigen CD44 on their surface. Expression of EpCAM, CD44, CD133, CD166, CD184 and CD24 on CSCs was studied by fow cytometry. Results. The CD45-EpCAMhighCD44+ colorectal cancer stem cells (CSCs) accounted for 17.15 % [11.76; 26.44] of the non-lymphoid cell population. Within this CSC population, 42.83 % [37.07; 51.77] simultaneously expressed CD133 and CD166, while 57.17 % [48.23; 62.93] expressed the CD133 antigen alone. All CSCs in the primary tumor expressed CD184, and 95.18 % [88.48; 97.98] of them simultaneously expressed CD24. The percentage of EpCAMhighCD44+ cells in well-differentiated tumors was 1.5 times lower than that in moderately-differentiated tumors (U=326.5, p=0.002) and 2.1 times lower than in poorly-differentiated tumors (U=21.0, p<0.001). In addition, the percentage of EpCAMhighCD44+CD133+CD166+ cells in stage IIIC CRC was 13 % higher than that in stage IIIB CRC (U=1116.0, p=0.007). Conclusion. In primary colorectal cancer tumors, cancer stem cells expressing high levels of EpCAM and CD44 accounted for 17.2 % of the non-lymphoid cell pool. The percentage of EpCAMhigh/CD44+ cells in poorly differentiated tumors was higher than that in well-or moderately-differentiated tumors.

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The authors declare that there are no conflicts of interest present.