DLEU2 facilitates bladder cancer progression through miR-103a-2-5p/SOS1 axis.

BACKGROUND

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.

METHODS

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.

RESULTS

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.

CONCLUSIONS

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.