Liu Yinlong, Hu Jian, Liao Baochun, Zhu Zhijian, Liu Yong, Pan Qinghua
Department of Abdominal Surgery, Ganzhou Cancer Hospital, Ganzhou, Jiangxi, China.
Department of Medical Oncology, Ganzhou Cancer Hospital, Ganzhou, Jiangxi, China.
PeerJ. 2025 Apr 8;13:e18995. doi: 10.7717/peerj.18995. eCollection 2025.
Bladder cancer (BC) represents a life-threatening malignancy within the urinary system. Dysregulated long non-coding RNAs (lncRNAs) play pivotal roles in the advancement of BC. LncRNA (DLEU2) is implicated in the development of various cancers. However, its role and regulatory mechanisms in BC remain unclear. This research aimed to explore the expression, biological function, and molecular mechanisms of In BC progression.
Expression profiles of lncRNAs, microRNAs (miRNAs), and mRNAs in normal and BC tissues were examined by leveraging the raw data sourced from the NCBI GEO database. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) validated expression levels in BC cells. To evaluate the proliferation and migration capabilities of BC cells, assays such as CCK-8, EdU, Transwell, and scratch were carried out. Luciferase reporter assays examined interactions between and miR-103a-2-5p and between miR-103a-2-5p with . Protein expression of in BC cells was analyzed western blotting.
was markedly increased in BC tissues. Functionally, overexpression elevated BC cell proliferation and migration, while its knockdown produced the opposite effects. Mechanistically, acted as a molecular sponge for miR-103a-2-5p, which targeted . miR-103a-2-5p knockdown enhanced proliferation and migration, while co-knockdown of miR-103a-2-5p and reversed these effects. Overexpression of also promoted proliferation and migration, which were counteracted by miR-103a-2-5p overexpression. Conversely, knockdown inhibited these processes, with miR-103a-2-5p knockdown reversing this inhibition.
These findings demonstrate that DLEU2 facilitates BC progression via the miR-103a-2-5p/SOS1 axis. This study reveals a novel regulatory mechanism underlying BC development and highlights DLEU2 as a potential therapeutic target for BC treatment.
膀胱癌（BC）是泌尿系统中一种危及生命的恶性肿瘤。长链非编码RNA（lncRNA）失调在膀胱癌的进展中起关键作用。LncRNA（DLEU2）与多种癌症的发生发展有关。然而，其在膀胱癌中的作用和调控机制仍不清楚。本研究旨在探讨DLEU2在膀胱癌进展中的表达、生物学功能及分子机制。
利用来自NCBI GEO数据库的原始数据检测正常和膀胱癌组织中lncRNAs、微小RNA（miRNAs）和信使RNA（mRNAs）的表达谱。逆转录定量聚合酶链反应（RT-qPCR）验证膀胱癌细胞中的表达水平。为评估膀胱癌细胞的增殖和迁移能力，进行了CCK-8、EdU、Transwell和划痕等实验。荧光素酶报告基因实验检测DLEU2与miR-103a-2-5p之间以及miR-103a-2-5p与SOS1之间的相互作用。通过蛋白质印迹法分析膀胱癌细胞中SOS1的蛋白表达。
DLEU2在膀胱癌组织中显著升高。在功能上，DLEU2过表达提高了膀胱癌细胞的增殖和迁移能力，而其敲低则产生相反的效果。机制上，DLEU2作为miR-103a-2-5p的分子海绵，而miR-103a-2-5p靶向SOS1。miR-103a-2-5p敲低增强了增殖和迁移，而miR-103a-2-5p和DLEU2共同敲低则逆转了这些作用。SOS1过表达也促进了增殖和迁移，而miR-103a-2-5p过表达则抵消了这些作用。相反，SOS1敲低抑制了这些过程，miR-103a-2-5p敲低则逆转了这种抑制。
这些发现表明，DLEU2通过miR-103a-2-5p/SOS1轴促进膀胱癌进展。本研究揭示了膀胱癌发生发展的一种新的调控机制，并突出了DLEU2作为膀胱癌治疗潜在靶点的作用。
