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hsa_circ_0058124 的敲低通过上调 miR-1297 抑制人肺癌细胞的增殖。

Knockdown of hsa_circ_0058124 inhibits the proliferation of human lung cancer cells by up-regulation of miR-1297.

机构信息

Department of Respiratory and Critical Care Medicine, Henan Provincial People's Hospital, Zhengzhou, China.

出版信息

Artif Cells Nanomed Biotechnol. 2020 Dec;48(1):584-593. doi: 10.1080/21691401.2020.1725537.

Abstract

Hsa_circ_0058124 was reported to possess the capacity of enhancing tumorigenesis and invasiveness. This investigation explored the effects of hsa_circ_0058124 on human lung cancer. qRT-PCR was employed for assessing the expression of hsa_circ_0058124 and miR-1297. Cell transfection was conducted for altering the expression of hsa_circ_0058124 and miR-1297. Dual-luciferase reporter gene assay was employed for exploring the relationship between hsa_circ_0058124 and miR-1297. CCK-8 assay, colony formation, flow cytometry, western blot and transwell assay were respectively conducted for exploring the effects of hsa_circ_0058124 silencing and miR-1297 inhibition. The expression of proteins participated in PTEN/AKT and Wnt/β-catenin pathways were determined for exploring the underlying mechanism. Hsa_circ_0058124 was highly expressed in human lung tumour tissues. Besides, hsa_circ_0058124 silencing suppressed cell viability, colony formation, migration and invasion, while enhanced cell apoptosis, which were respectively verified by the regulation of apoptosis-associated and metastasis-related proteins. Additionally, hsa_circ_0058124 silencing inhibited the expression of proteins involved in PTEN/AKT and Wnt/β-catenin pathways including p/t-AKT and β-catenin. miR-1297 was lowly expressed in patients' tumour tissues and was a target of hsa_circ_0058124. Moreover, the above mentioned effects were prominently abrogated by miR-1297 inhibition. This research verified that hsa_circ_0058124 silencing might achieve its anti-tumour roles via inactivation of PTEN/AKT and Wnt/β-catenin pathways through elevating miR-1297 expression.

摘要

Hsa_circ_0058124 被报道具有增强肿瘤发生和侵袭的能力。本研究探讨了 hsa_circ_0058124 对人肺癌的影响。qRT-PCR 用于评估 hsa_circ_0058124 和 miR-1297 的表达。细胞转染用于改变 hsa_circ_0058124 和 miR-1297 的表达。双荧光素酶报告基因检测用于探讨 hsa_circ_0058124 和 miR-1297 之间的关系。CCK-8 检测、集落形成、流式细胞术、Western blot 和 Transwell 检测分别用于探讨 hsa_circ_0058124 沉默和 miR-1297 抑制的影响。测定参与 PTEN/AKT 和 Wnt/β-catenin 通路的蛋白表达,探讨其潜在机制。hsa_circ_0058124 在人肺癌组织中高表达。此外,hsa_circ_0058124 沉默抑制细胞活力、集落形成、迁移和侵袭,同时增强细胞凋亡,这分别通过调节凋亡相关和转移相关蛋白得到验证。此外,hsa_circ_0058124 沉默抑制了参与 PTEN/AKT 和 Wnt/β-catenin 通路的蛋白表达,包括 p/t-AKT 和 β-catenin。miR-1297 在患者肿瘤组织中低表达,是 hsa_circ_0058124 的靶点。此外,miR-1297 抑制显著削弱了上述作用。本研究证实,hsa_circ_0058124 沉默可能通过上调 miR-1297 表达,通过失活 PTEN/AKT 和 Wnt/β-catenin 通路来发挥其抗肿瘤作用。

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