Journal of cancer research and clinical oncology · 2025
tRF-34-86J8WPMN1E8Y2Q promotes the occurrence and development of gastric cancer by combining with LRAT.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
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.
Cao Chunli, Xu Shengli, Li Zhe
Аннотация
BACKGROUND: A large number of studies have demonstrated that tRNA-derived fragments (tRFs) are implicated in the progression and nociception associated with various malignancies. However, the biological role of tRF-34-86J8WPMN1E8Y2Q (tRF-34) in cancer, particularly in gastric cancer (GC), remains elusive and warrants investigation. This study aimed to investigate the clinical and mechanistic significance of tRF-34 in GC pathogenesis and potential as novel biomarker for early detection.
METHODS: The quantitative expression levels of tRF-34 in GC cell lines, tissues, and plasma were determined using quantitative real-time polymerase chain reaction (qRT-PCR). Subsequently, the functional impact of tRF-34 downregulation on GC progression was investigated using Cell Counting Kit-8 (CCK-8) assays to assess cell proliferation and transwell assays to evaluate migration and invasion. Downstream target genes of tRF-34 were identified through database analysis and validated using RNA Binding Protein Immunoprecipitation (RIP) experiments.
RESULTS: tRF-34 exhibits elevated expression levels in GC tissues cells and preoperative (1 day) plasma compared with normal counterparts and postoperative (10 day) plasma. Also, it was associated with neural and vascular invasion in patients with GC. Moreover, tRF-34 downregulation impedes the proliferative, migratory, and invasive capacities of GC cells. Mechanistically, RIP and bioinformatic analyses demonstrated that tRF-34 directly bound to lecithin retinol acyltransferase (LRAT), and this interaction promoted the progression of GC.
CONCLUSION: tRF-34 has high expression specificity in GC and the potential to be a biomarker for early detection. Also, tRF-34 directly binds to LRAT, facilitating GC progression.
METHODS: The quantitative expression levels of tRF-34 in GC cell lines, tissues, and plasma were determined using quantitative real-time polymerase chain reaction (qRT-PCR). Subsequently, the functional impact of tRF-34 downregulation on GC progression was investigated using Cell Counting Kit-8 (CCK-8) assays to assess cell proliferation and transwell assays to evaluate migration and invasion. Downstream target genes of tRF-34 were identified through database analysis and validated using RNA Binding Protein Immunoprecipitation (RIP) experiments.
RESULTS: tRF-34 exhibits elevated expression levels in GC tissues cells and preoperative (1 day) plasma compared with normal counterparts and postoperative (10 day) plasma. Also, it was associated with neural and vascular invasion in patients with GC. Moreover, tRF-34 downregulation impedes the proliferative, migratory, and invasive capacities of GC cells. Mechanistically, RIP and bioinformatic analyses demonstrated that tRF-34 directly bound to lecithin retinol acyltransferase (LRAT), and this interaction promoted the progression of GC.
CONCLUSION: tRF-34 has high expression specificity in GC and the potential to be a biomarker for early detection. Also, tRF-34 directly binds to LRAT, facilitating GC progression.