# Mechanistic insights into miR-4775-mediated regulation of pancreatic cancer cell invasion and migration through BRMS1L

## TL;DR

This study shows that miR-4775 promotes pancreatic cancer progression by reducing BRMS1L, which affects cancer cell growth, migration, and invasion.

## Contribution

The study identifies miR-4775 as a novel regulator of pancreatic cancer via its direct targeting of BRMS1L.

## Key findings

- miR-4775 is overexpressed in pancreatic cancer tissues and linked to worse patient outcomes.
- Inhibiting miR-4775 reduces cancer cell viability, migration, and invasion.
- BRMS1L knockdown reverses the effects of miR-4775 inhibition, confirming its regulatory role.

## Abstract

This study aims to investigate the effects of miR-4775 on pancreatic cancer cell (PC) invasion and migration, and to elucidate the underlying molecular mechanisms.

Quantitative Real-Time Reverse Transcription (RT-qPCR) was performed to analyze miR-4775 and BRMS1L expression levels in both human PC tissues and human pancreatic carcinoma cells‌ (PANC-1) lines. The prognostic value of miR-4775 in PC patients was evaluated through survival analysis. The CCK-8 assay was employed to assess cell viability, while Transwell assays were utilized to evaluate invasion and migration capabilities. The regulatory interaction between miR-4775 and BRMS1L was confirmed by dual-luciferase reporter assay.

Comparative analysis revealed significantly elevated miR-4775 expression in PC tissues versus adjacent normal tissues, with high miR-4775 expression correlating with poorer patient prognosis. Functional studies demonstrated that inhibition of miR-4775 significantly attenuated cellular viability, migration, and invasion capabilities, while knockdown of breast cancer metastasis suppressor 1-like‌ (BRMS1L) effectively rescued these suppressive effects. The luciferase reporter assay confirmed a direct negative regulatory relationship between miR-4775 and its target gene BRMS1L.

These findings demonstrate that miR-4775 regulates PC progression by modulating cancer cell viability, migration, and invasion through BRMS1L-mediated mechanisms.