medgenМедицинская генетикаMedical Genetics2073-7998Publishing House «Genius Media» LLC10.25557/2073-7998.2024.11.40-46medgen-2572Research ArticleОРИГИНАЛЬНЫЕ ИССЛЕДОВАНИЯORIGINAL RESEARCHПрименение технологии CRISPR/Cas для создания сублинии клеток рака легкого А549 с нокаутом гена E2F1Using CRISPR/Cas technology to generate A549 human lung cancer subline with knockout of the E2F1 geneЗамковаМ. А.ZamkovaМ. А.

Замкова М.А.

119334, г. Москва, ул. Вавилова, д. 34/5

34/5, Vavilova st., Moscow, 119334;

23, Kashirskoe shosse, Moscow, 115522

zamkovam@gmail.comКазанскийД. Б.KazanskyD. B.

115522, г. Москва, Каширское шоссе, д. 23

23, Kashirskoe shosse, Moscow, 115522

ТатарскийВ. В.TatarskiyV. V.

119334, г. Москва, ул. Вавилова, д. 34/5

34/5, Vavilova st., Moscow, 119334

Институт биологии гена Российской академии наукРоссияInstitute of Gene Biology, Russian Academy of Sciences; National Medical Research Center of Oncology named after N.N. Blokhin of the Ministry of Health of the Russian FederationRussian FederationФГБУ Национальный медицинский исследовательский центр онкологии им. Н.Н. Блохина Минздрава РоссииРоссияNational Medical Research Center of Oncology named after N.N. Blokhin of the Ministry of Health of the Russian FederationRussian FederationИнститут биологии гена Российской академии наукРоссияInstitute of Gene Biology, Russian Academy of SciencesRussian Federation20240501202523114046Copyright © Замкова М.А., Казанский Д.Б., Татарский В.В., 20252025Замкова М.А., Казанский Д.Б., Татарский В.В.Zamkova М.А., Kazansky D.B., Tatarskiy V.V.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://www.medgen-journal.ru/jour/article/view/2572

Несмотря на значительное количество исследований, посвященных транскрипционному фактору E2F1, его функциональная роль в клеточных процессах остаётся неоднозначной. В зависимости от контекста E2F1 может либо поддерживать выживание клеток, либо инициировать апоптоз. Настоящая работа посвящена рассмотрению возможности использования E2F1 в качестве терапевтической мишени для комбинированного лечения злокачественных новообразований, в том числе через применение ингибиторов. Однако имеющиеся данные также свидетельствуют о потенциально противоположном эффекте E2F1, способном негативно влиять на эффективность терапии. Это подчёркивает актуальность углублённого изучения функциональной активности E2F1 в различных условиях. Факторы транскрипции семейства E2F, включая E2F1, демонстрируют как пересекающиеся функции, так и уникальные свойства, присущие отдельным его членам. Подавление экспрессии отдельных представителей семейства даёт возможность более точно оценить их вклад в ключевые клеточные процессы. В рамках проведённого исследования была разработана сублиния клеток рака лёгкого A549 с нокаутом гена E2F1, осуществлённым с использованием технологии CRISPR/ Cas. На основе данной клеточной модели планируется проведение экспериментов, направленных на изучение роли E2F1 в различных условиях, включая реакции на химиотерапевтические воздействия

Despite a significant number of studies devoted to the transcription factor E2F1, its functional role in cellular processes remains ambiguous. Depending on the context, E2F1 can either support cell survival or initiate apoptosis. The present work is devoted to the possibility of using E2F1 as a therapeutic target for the combined treatment of malignant neoplasms, including through the use of inhibitors. However, the available data also indicate a potentially opposite effect of E2F1, which can negatively affect the effectiveness of therapy. This emphasizes the relevance of an in-depth study of the functional activity of E2F1 in various conditions. Transcription factors of the E2F family, including E2F1, demonstrate both overlapping functions and unique properties inherent in its individual members. Suppression of the expression of individual representatives of the family makes it possible to more accurately assess their contribution to key cellular processes. As part of the study, a subline of A549 lung cancer cells with a knockout of the E2F1 gene, carried out using CRISPR/Cas technology, was developed. Based on this cell model, experiments are planned to be carried out aimed at studying the role of E2F1 in various conditions, including responses to chemotherapeutic effects

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