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

## TL;DR

This study shows that the lncRNA DLEU2 promotes bladder cancer growth by interacting with miR-103a-2-5p and SOS1, suggesting a new target for treatment.

## Contribution

The study identifies a novel regulatory mechanism involving DLEU2, miR-103a-2-5p, and SOS1 in bladder cancer progression.

## Key findings

- DLEU2 overexpression increases bladder cancer cell proliferation and migration.
- DLEU2 acts as a sponge for miR-103a-2-5p, which targets SOS1 to regulate cancer progression.
- SOS1 overexpression promotes cancer cell growth, which is counteracted by miR-103a-2-5p.

## Abstract

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 deleted in lymphocytic leukemia 2 (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 DLEU2 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 DLEU2 and miR-103a-2-5p and between miR-103a-2-5p with SOS1. Protein expression of SOS1 in BC cells was analyzed via western blotting.

DLEU2 was markedly increased in BC tissues. Functionally, DLEU2 overexpression elevated BC cell proliferation and migration, while its knockdown produced the opposite effects. Mechanistically, DLEU2 acted as a molecular sponge for miR-103a-2-5p, which targeted SOS1. miR-103a-2-5p knockdown enhanced proliferation and migration, while co-knockdown of miR-103a-2-5p and DLEU2 reversed these effects. Overexpression of SOS1 also promoted proliferation and migration, which were counteracted by miR-103a-2-5p overexpression. Conversely, SOS1 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.