| 摘要: |
| ［摘要］ 目的 研究lncRNA SNHG16通过结合STAU1降低PRKN mRNA稳定性促进乳腺癌放射抗拒的机制。方法 通过TCGA数据库分析lncRNA SNHG16在乳腺癌组织中的表达。采用实时荧光定量聚合酶链反应（RT-qPCR）检测lncRNA SNHG16在乳腺癌细胞中的表达。选择lncRNA SNHG16高表达的MDA-MB-231和MCF-7细胞进行转染，分成si-NC组（对照组）和si-SNHG16组（实验组）。转染48 h后取对数生长期细胞开展实验。CCK-8实验检测细胞增殖，流式细胞术检测细胞凋亡，Transwell实验检测细胞侵袭，CCK-8实验检测细胞放射敏感性，葡萄糖摄取比色分析试剂盒测定细胞葡萄糖摄取量，RNA免疫沉淀（RIP）检测结合mRNA稳定性实验验证lncRNA SNHG16、STAU1、PRKN之间的调控关系。结果 lncRNA SNHG16在乳腺癌组织和细胞中高表达，敲减lncRNA SNHG16表达逆转了乳腺癌细胞的增殖、凋亡、侵袭和放射抗拒，并抑制乳腺癌细胞的糖代谢重编程。RIP实验证实STAU1与PRKN mRNA存在相互作用，而敲减lncRNA SNHG16表达可以减弱这种相互作用，敲减STAU1表达可以增强PRKN mRNA的稳定性。结论 乳腺癌细胞中高表达的lncRNA SNHG16结合STAU1，通过转录后修饰途径降低PRKN mRNA的稳定性，进而影响糖代谢重编程，促进乳腺癌的放射抗拒。 |
| 关键词: 乳腺癌放射抗拒 糖代谢 lncRNA SNHG16 STAU1 PRKN |
| DOI：10.3969/j.issn.1674-3806.2025.10.11 |
| 分类号: |
| 基金项目:海南省自然科学基金青年基金项目（编号：821QN393） |
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| Study on mechanisms of lncRNA SNHG16 promoting breast cancer radioresistance by binding to STAU1 to reduce the stability of PRKN mRNA |
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ZHONG Rui1, CHEN Ru2
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1.Department of Radiotherapy, Hainan General Hospital(Hainan Affiliated Hospital of Hainan Medical University), Haikou 570311, China; 2.Department of Breast Surgery, Hainan General Hospital(Hainan Affiliated Hospital of Hainan Medical University), Haikou 570311, China
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| Abstract: |
| ［Abstract］ Objective To study the mechanisms of long non-coding ribonucleic acid(RNA)(lncRNA) small nucleolar RNA host gene 16(SNHG16) promoting breast cancer radioresistance by binding to host cellular RNA binding protein Staufen 1(STAU1) to reduce the stability of Parkin RBR E3 ubiquitin protein ligase(PRKN) mRNA. Methods The expressions of lncRNA SNHG16 in breast cancer tissues were analyzed by using The Cancer Genome Atlas(TCGA) database and real-time quantitative polymerase chain reaction(RT-qPCR) was used to detect the expressions of lncRNA SNHG16 in breast cancer cells. MDA-MB-231 and MCF-7 cells with high expression of lncRNA SNHG16 were selected for transfection and were divided into si-NC group(control group) and si-SNHG16 group(experimental group). Cells in logarithmic growth phase were taken for experiment 48 hours after transfection. Cell proliferation was detected by using Cell Counting Kit-8(CCK-8) assay. Cell apoptosis was detected by using flow cytometry. Cell invasion was detected by using Transwell assay. Cell radiosensitivity was detected by using CCK-8 assay. Cellular glucose uptake was determined by using the glucose uptake colorimetric assay kit. The combination of RNA immunoprecipitation(RIP) detection with RNA stability experiment was used to verify the regulatory relationship among lncRNA SNHG16, STAU1 and PRKN. Results lncRNA SNHG16 was highly expressed in breast cancer tissues and cells. Knockdown of lncRNA SNHG16 expression reversed the proliferation, apoptosis, invasion and radioresistance of the breast cancer cells, and inhibited the reprogramming of glucose metabolism in breast cancer cells. The RIP experiment confirmed that there was an interaction between STAU1 and PRKN mRNA, whereas knockdown of lncRNA SNHG16 attenuated this interaction relationship, and knockdown of STAU1 expression also enhanced the stability of PRKN mRNA. Conclusion The highly expressing lncRNA SNHG16 in breast cancer cells binding to STAU1 reduces the stability of PRKN mRNA via a post-transcriptional modification pathway, thus affecting the reprogramming of glucose metabolism and promoting radioresistance in breast cancer. |
| Key words: Breast cancer radioresistance Glycometabolism Long non-coding ribonucleic acid small nucleolar ribonucleic acid host gene 16(lncRNA SNHG16) Host cellular RNA binding protein Staufen 1(STAU1) Parkin RBR E3 ubiquitin protein ligase(PRKN) |
