# Prognostic significance of LINC01132 in lung cancer and its regulatory role in tumor progression

## TL;DR

This study shows that LINC01132, a long non-coding RNA, is linked to lung cancer progression and patient survival, acting through miR-125a-3p and SMAD2.

## Contribution

The study identifies LINC01132 as a novel prognostic biomarker and functional regulator in lung cancer via the miR-125a-3p/SMAD2 pathway.

## Key findings

- LINC01132 is upregulated in lung cancer tissues and is an independent risk factor for poor survival.
- LINC01132 knockdown reduces cancer cell proliferation and migration by targeting miR-125a-3p and SMAD2.
- SMAD2 knockdown reverses the effects of miR-125a-3p inhibition on cancer cell behavior.

## Abstract

The application of long non-coding RNAs (lncRNAs) in cancer has been the focus of research in recent years. This study aimed to discuss the expression and functional mechanism of lncRNA LINC01132 (LINC01132) in lung cancer and explore its prognostic significance in tumors.

The expression of LINC01132 in lung cancer patients was verified using GSE98929 screening and real-time quantitative polymerase chain reaction (RT-qPCR) detection. The prognostic potential of LINC01132 was evaluated by performing the chi-square analysis of clinical indicators, Kaplan–Meier analysis, and Cox proportional hazard model. Cell Counting Kit-8 (CCK-8), flow cytometry, and Transwell assay were used to characterize the biological functions of the lung cancer cells. The targeting relationship between LINC01132 and microRNA-125a-3p (miR-125a-3p), miR-125a-3p and SMAD2 was predicted by bioinformatics and verified by luciferase activity assay.

LINC01132 was upregulated in lung cancer tissues and cells, which was an independent risk factor for survival and prognostic outcomes of lung cancer patients. Silencing LINC01132 suppressed the proliferation and migration of lung cancer cells and accelerated cell death. The target of LINC01132 was miR-125a-3p, and miR-125a-3p inhibitor could eliminate the inhibitory effect of LINC01132 knockdown on the cells. Additionally, SMAD2 is a downstream target of miR-125a-3p, and knockdown of SMAD2 reversed the effects of miR-125a-3p inhibitor on cell migration and invasion.

LINC01132 may regulate the progression of lung cancer by targeting the miR-125a-3p /SMAD2 axis and serve as a prognostic biomarker for lung cancer.