DNA and cell biology · 2026
Compensatory Gene Regulation Following Survivin Inhibition in MDA-MB-231 Cells.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Martínez-Sifuentes Manuel Antonio, Ramos-Treviño Juan, Espinosa-Castilla Magali, Villa-Cedillo Sheila Adela, Encino-Ortega Iliana, Muñoz-Dominguez Michelle Alejandra, Ruiz-Flores Pablo, Hernández-Ibarra José Anselmo
Аннотация
Breast cancer is the most diagnosed cancer in women and the second leading cause of cancer-related mortality worldwide. Advances in genetic technology have highlighted the heterogeneity of breast cancer, composed of various biological subtypes, with genetic profiling playing a crucial role in predicting chemotherapy response. This underscores the importance of identifying sensitive diagnostic and prognostic markers for early detection and developing more efficient targeted therapies. Among these, survivin, a protein linked to apoptosis inhibition and cell cycle regulation, is strongly expressed in various cancers, including breast cancer, where its overexpression is associated with poor prognosis and reduced survival rates. To analyze the effects of survivin gene inhibition in a triple-negative breast cancer (TNBC) model. The MDA-MB-231 cell line was stably transfected with short hairpin RNA targeting survivin, and the inhibition was validated via RT-qPCR and Western blot. Morphological evaluation, proliferation and migration assays, and a differential gene expression analysis using the GeneChip™ Human Gene 2.0 ST Array were performed. Statistical analyses were conducted with GraphPad Prism version 8 and Transcriptome Analysis Console. Survivin-inhibited MDA-MB-231-KD cells exhibited evident morphological changes, reduced migration capacity, and altered expression of genes such as BCL2, COX1, COX2, VGF, BIR2, and CDC20, involved in key cancer signaling pathways. Inhibition of survivin in this TNBC model induces critical cellular changes and significantly alters gene expression associated with tumor progression, highlighting its potential as a therapeutic target.