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DOI 10.1016/j.clinre.2024.102398

Медицинская библиотека · Clinics and research in hepatology and gastroenterology · 2024

Clinical significance of lncRNA XIST expression in cholangiocarcinoma and its effect on cell migration and invasion.

Li Chenxi, Dong Yifei, Zhang Yichuan, Wu Caihong

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Аннотация

BACKGROUND

Cholangiocarcinoma is a malignant tumor that occurs in the bile duct system, and the prognosis of patients is poor. Currently, research suggests that long non-coding RNAs (lncRNAs) in the treatment and prevention of cholangiocarcinoma. This study primarily focuses on the regulation and potential mechanism of the lncRNA XIST (XIST) in cholangiocarcinoma.

METHODS

The levels of XIST and miR-126-3p in cholangiocarcinoma tissues and cells were detected using real-time quantitative polymerase chain reaction (RT-qPCR). Cell transfection status, including migration and invasion, was examined via the Transwell method. The relationship between XIST and miR-126-3p was observed by dual-luciferase gene reporter assay and verified by rescue assays. Additionally, the prognostic significance of XIST in cholangiocarcinoma was determined using Kaplan-Meier and multivariate Cox regression analyses.

RESULTS

XIST expression was increased in cholangiocarcinoma, while miR-126-3p was decreased, in both tissues and cells. The successful construction of silencing XIST was found to inhibit the count of cell migration and invasion. XIST directly targeted miR-126-3p to regulate the progression of cholangiocarcinoma.

CONCLUSION

XIST sponging miR-126-3p inhibited the progression of cholangiocarcinoma and improved the prognosis for patients. This finding provides new insights and opportunities for future studies on cholangiocarcinoma prognostic biomarkers.

Для цитирования: Li Chenxi, Dong Yifei, Zhang Yichuan, Wu Caihong. Clinical significance of lncRNA XIST expression in cholangiocarcinoma and its effect on cell migration and invasion.. Clinics and research in hepatology and gastroenterology. 2024. DOI: 10.1016/j.clinre.2024.102398.

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