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IGF2BP3 loss inhibits cell progression by upregulating has_circRNA_103820, and hsa_circRNA_103820-encoded peptide inhibits cell progression by inactivating the AKT pathway in lung cancer
Chemical Biology & Drug Design ( IF 3 ) Pub Date : 2024-02-20 , DOI: 10.1111/cbdd.14473
Jinrong Zhou 1 , Lixia Yao 1 , Yuan Su 2 , Lili Tian 3
Affiliation  

N6-methyladenosine (m6A) modification and m6A-related RNA-binding proteins (RBPs) play vital roles in various aspects of circRNA metabolism. Hsa_circRNA_103820 is implicated in the pathogenesis of multiple cancers, including lung cancer (LC). Moreover, bioinformatics analysis has suggested that hsa_circRNA_103820 possesses potential peptide-coding ability. Thus, we aimed to investigate the function and peptide-coding potential of hsa_circRNA_103820 in this study. Cell viability, apoptosis rate, and migratory and invasive abilities were assessed using CCK-8, flow cytometry, and transwell assays, respectively. Hsa_circRNA_103820 level was measured using RT-qPCR assay, and the interaction between hsa_circRNA_103820 and IGF2BP3 was examined through RIP and RT-qPCR assays. The coding ability of hsa_circRNA_103820 and protein levels were determined through western blot assay. The results showed that hsa_circRNA_103820 reduced cell viability, attenuated cell migratory and invasive abilities, and promoted cell apoptosis in LC. IGF2BP3 negatively regulated hsa_circRNA_103820 expression and interacted with it. Hsa_circRNA_103820 knockdown alleviated si-IGF2BP3-mediated anti-viability, anti-migration, anti-invasion, and pro-apoptosis effects in LC cells. Moreover, a 188-amino acid (aa) peptide encoded by hsa_circRNA_103820 decreased cell viability, facilitated cell apoptosis, and inhibited cell migration and invasion in LC. Collectively, hsa_circRNA_103820, regulated by IGF2BP3, encodes a 188-aa peptide and inhibits the malignant progression of LC cells by inhibiting the AKT pathway.

中文翻译:

IGF2BP3 缺失通过上调 has_circRNA_103820 抑制细胞进展,hsa_circRNA_103820 编码肽通过失活肺癌中的 AKT 通路抑制细胞进展

N6-甲基腺苷 (m6A) 修饰和 m6A 相关 RNA 结合蛋白 (RBP) 在 circRNA 代谢的各个方面发挥着重要作用。Hsa_circRNA_103820 与多种癌症的发病机制有关,包括肺癌 (LC)。此外,生物信息学分析表明hsa_circRNA_103820具有潜在的肽编码能力。因此,我们的目的是在本研究中研究 hsa_circRNA_103820 的功能和肽编码潜力。分别使用 CCK-8、流式细胞术和 Transwell 测定来评估细胞活力、凋亡率以及迁移和侵袭能力。使用RT-qPCR测定测量hsa_circRNA_103820水平,并通过RIP和RT-qPCR测定检查hsa_circRNA_103820和IGF2BP3之间的相互作用。通过蛋白质印迹法测定hsa_circRNA_103820的编码能力和蛋白水平。结果表明,hsa_circRNA_103820在LC中降低细胞活力,减弱细胞迁移和侵袭能力,并促进细胞凋亡。IGF2BP3 负向调节 hsa_circRNA_103820 表达并与其相互作用。Hsa_circRNA_103820 敲低减轻了 si-IGF2BP3 介导的 LC 细胞中的抗活力、抗迁移、抗侵袭和促凋亡作用。此外,hsa_circRNA_103820 编码的 188 个氨基酸 (aa) 肽可降低细胞活力,促进细胞凋亡,并抑制细胞迁移和侵袭。总的来说,hsa_circRNA_103820受IGF2BP3调节,编码188个氨基酸的肽,并通过抑制AKT途径来抑制LC细胞的恶性进展。
更新日期:2024-02-23
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