RBM15-mediated m6A modification of XPR1 promotes the malignant progression of lung adenocarcinoma.

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Tác giả: Yinfeng Gu, Hongjun Guan, Jinjin Li, Changpeng Sun

Ngôn ngữ: eng

Ký hiệu phân loại:

Thông tin xuất bản: Germany : Naunyn-Schmiedeberg's archives of pharmacology , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 5273

Lung adenocarcinoma (LUAD) is a leading cause of cancer-related deaths worldwide. The poor prognosis of LUAD is attributed to its aggressive biological behavior and resistance to conventional therapies. Xenotropic and polytropic retrovirus receptor 1 (XPR1), a member of the XPR family, has been implicated in the pathogenesis of various malignancies, including LUAD. However, the regulatory mechanism of XPR1 in LUAD remains elusive. The study employed immunohistochemistry (IHC) and western blotting to analyze the protein expression of XPR1, RNA binding motif protein 15 (RBM15) and nuclear proliferation marker (ki-67) in LUAD tissues and cells. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the mRNA expression of XPR1, glutathione peroxidase 4 (GPX4), solute carrier family 7 member 11 (SLC7A11), and RBM15. Cell proliferation was assessed using a CCK-8 assay, colony-formation assay, and 5-Ethynyl-2'-deoxyuridine assay. Cell invasion and apoptosis were evaluated through transwell assay and flow cytometry, respectively. Caspase 3 activity and Fe
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