LncRNA EBLN3P Accelerates Cell Proliferation and Invasion of Colon Cancer through Modulating the miR-519d-3p/ZFP91 Axis.

Xiaohui Wang, Yinzi Yue, Jinhua Tan, Fei Kou, Bude Su, Jin Xie, Shuai Yan
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Abstract

Purpose: The study aims to explore the roles and underlying mechanisms of long noncoding RNAs endogenous bornavirus-like nucleoprotein (lncRNA EBLN3P) in colon cancer, emphasizing the potential impact of these insights on advancing colon cancer treatment strategies. By shedding light on lncRNA EBLN3P's involvement, this research could contribute to the development of novel therapeutic approaches, enhancing the efficacy of interventions for colon cancer patients. Methods: We employed quantitative reverse transcription polymerase chain reaction to assess the levels of lncRNA EBLN3P, zinc finger protein (ZFP91), and miR-519d-3p, alongside CCK-8 and EdU assays for cell proliferation, flow cytometry for apoptosis, and Transwell and wound healing assays for migration and invasion. The in vivo function of lncRNA EBLN3P was investigated through a xenograft model, and protein levels were evaluated via Western blot analysis. Results: LncRNA EBLN3P was found to be upregulated in colon cancer tissues and cells, promoting cell proliferation and metastasis while inhibiting apoptosis. Downregulation of lncRNA EBLN3P reduced tumor size, volume, and weight in a mouse model. MiR-519d-3p, which negatively interacts with lncRNA EBLN3P, was found to be downregulated in colon cancer tissues and cell lines. Its upregulation hindered cancer cell proliferation and metastasis while enhancing apoptosis. ZFP91, a binding partner of miR-519d-3p, was upregulated in colon cancer and inversely related to miR-519d-3p levels. Rescue experiments indicated that the effects of lncRNA EBLN3P silencing could be reversed by miR-519d-3p suppression, but were mitigated by ZFP91 downregulation. Conclusion: LncRNA EBLN3P facilitates colon cancer progression via the miR-519d-3p/ZFP91 axis, presenting a novel understanding of lncRNA EBLN3P's role and offering potential therapeutic insights for colon cancer treatment. This study fills a critical gap by linking lncRNA EBLN3P with the miR-519d-3p/ZFP91 axis in the context of colon cancer, thereby broadening our understanding of the molecular mechanisms underlying colon cancer progression.
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LncRNA EBLN3P通过调节miR-519d-3p/ZFP91轴加速结肠癌细胞增殖和侵袭
目的:本研究旨在探索长非编码RNA内源性天生病毒样核蛋白(lncRNA EBLN3P)在结肠癌中的作用和潜在机制,强调这些见解对推进结肠癌治疗策略的潜在影响。通过揭示lncRNA EBLN3P的参与,这项研究可促进新型治疗方法的开发,提高结肠癌患者的干预疗效。研究方法我们采用定量反转录聚合酶链反应来评估lncRNA EBLN3P、锌指蛋白(ZFP91)和miR-519d-3p的水平,同时采用CCK-8和EdU检测法检测细胞增殖,流式细胞术检测细胞凋亡,Transwell和伤口愈合检测法检测迁移和侵袭。通过异种移植模型研究了lncRNA EBLN3P的体内功能,并通过Western印迹分析评估了蛋白水平。结果研究发现,LncRNA EBLN3P在结肠癌组织和细胞中上调,促进细胞增殖和转移,同时抑制细胞凋亡。在小鼠模型中,下调lncRNA EBLN3P可减少肿瘤的大小、体积和重量。研究发现,在结肠癌组织和细胞系中,与lncRNA EBLN3P有负作用的MiR-519d-3p被下调。它的上调阻碍了癌细胞的增殖和转移,同时增强了细胞凋亡。ZFP91是miR-519d-3p的结合伙伴,在结肠癌中上调,并与miR-519d-3p水平成反比。拯救实验表明,抑制miR-519d-3p可逆转lncRNA EBLN3P沉默的影响,但ZFP91的下调可减轻这种影响。结论LncRNA EBLN3P通过miR-519d-3p/ZFP91轴促进结肠癌的进展,为lncRNA EBLN3P的作用提供了新的认识,并为结肠癌治疗提供了潜在的治疗见解。这项研究填补了一项重要空白,将结肠癌中的lncRNA EBLN3P与miR-519d-3p/ZFP91轴联系起来,从而拓宽了我们对结肠癌进展的分子机制的认识。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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Theranostics: Timing is Everything. Short-Term Biological Toxicity Prediction of [177Lu]Lutetium-Oxodotreotide: An Original Retrospective Analysis. LncRNA EBLN3P Accelerates Cell Proliferation and Invasion of Colon Cancer through Modulating the miR-519d-3p/ZFP91 Axis. Acknowledgment of Reviewers 2023.
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