长链非编码RNA PRSS23-AS1作为ceRNA通过miR-3176/YBX1轴调控EMT促进乳腺癌进展
Long non-coding RNA PRSS23-AS1 as ceRNA promotes breast cancer progression by regulating EMT via miR-3176 /YBX1 axis
原文发布日期:2025-07-24
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Breast cancer (BC) remains a leading cause of cancer-related mortality, largely due to its aggressive proliferation and metastatic potential. Long non-coding RNAs (lncRNAs) have emerged as key regulators in tumor development and progression. This study explored the functional role and mechanism of Lnc-PRSS23-AS1 in BC. We assessed Lnc-PRSS23-AS1 expression and localization using fluorescence in situ hybridization, qRT-PCR, and Western blotting in BC tissues and cell lines. Binding interactions between Lnc-PRSS23-AS1, miR-3176, and Y-box binding protein 1 (YBX1) were validated through dual-luciferase reporter assays, RNA pulldown, and RNA immunoprecipitation. Lnc-PRSS23-AS1 was significantly upregulated in BC and predominantly localized in the cytoplasm. Silencing Lnc-PRSS23-AS1 or overexpressing miR-3176 suppressed BC cell proliferation, migration, and invasion in vitro and in vivo. Conversely, miR-3176 inhibition or YBX1 overexpression reversed these effects. Mechanistically, Lnc-PRSS23-AS1 promoted YBX1 protein expression by acting as a molecular sponge for miR-3176. These findings highlight the Lnc-PRSS23-AS1/miR-3176/YBX1 axis as a driver of BC progression and suggest Lnc-PRSS23-AS1 as a potential therapeutic target for breast cancer treatment.
乳腺癌(BC)仍是癌症相关死亡的主要原因,这主要归因于其侵袭性增殖和转移潜能。长链非编码RNA(lncRNA)已成为肿瘤发生发展过程中的关键调控因子。本研究探讨了Lnc-PRSS23-AS1在乳腺癌中的功能作用及机制。我们通过荧光原位杂交、qRT-PCR和Western blotting技术检测了Lnc-PRSS23-AS1在乳腺癌组织和细胞系中的表达及定位;通过双荧光素酶报告基因实验、RNA pulldown和RNA免疫沉淀验证了Lnc-PRSS23-AS1与miR-3176、Y盒结合蛋白1(YBX1)之间的结合作用。Lnc-PRSS23-AS1在乳腺癌中显著上调且主要定位于细胞质。沉默Lnc-PRSS23-AS1或过表达miR-3176可在体内外抑制乳腺癌细胞增殖、迁移和侵袭;相反,抑制miR-3176或过表达YBX1可逆转这些效应。机制上,Lnc-PRSS23-AS1通过作为miR-3176的分子海绵促进YBX1蛋白表达。这些发现揭示了Lnc-PRSS23-AS1/miR-3176/YBX1轴是驱动乳腺癌进展的关键通路,表明Lnc-PRSS23-AS1可能成为乳腺癌治疗的潜在靶点。
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