# Aloe-emodin mediates the inhibitory effect of LncRNA D63785 on the PI3K/Akt/mTOR pathway in nasopharyngeal carcinoma

## TL;DR

This study shows that aloe-emodin fights nasopharyngeal cancer by reducing a specific lncRNA and inhibiting a key cancer-related pathway.

## Contribution

The study reveals a novel mechanism where aloe-emodin targets lncRNA D63785 to inhibit the PI3K/Akt/mTOR pathway in NPC.

## Key findings

- LncRNA D63785 is overexpressed in NPC cells and is suppressed by aloe-emodin.
- Aloe-emodin reduces PI3K/Akt/mTOR pathway activity, which is linked to decreased cancer cell proliferation and migration.
- In vivo experiments show aloe-emodin reduces tumor growth by downregulating lncRNA D63785 and dephosphorylating the pathway.

## Abstract

Long non-coding RNAs (lncRNAs) are dysregulated in nasopharyngeal carcinoma (NPC), yet their interplay with pharmacological agents like aloe-emodin (AE) remains unclear. This study explores AE’s anti-NPC mechanisms via lncRNA D63785 and the PI3K/Akt/mTOR pathway.

NPC cells (CNE1, C666-1) were treated with AE, followed by qRT-PCR and Western blotting to assess lncRNA D63785 and PI3K/Akt/mTOR pathway proteins. siRNA-mediated lncRNA D63785 knockdown combined with functional assays (CCK-8, EdU, colony/wound-healing) evaluated AE’s effects on proliferation, migration, and pathway activity. In vivo validation used nude mouse xenografts.

LncRNA D63785 was overexpressed in NPC cells (p < 0.01). AE suppressed lncRNA D63785 expression, concurrently reducing PI3K/Akt/mTOR phosphorylation (p < 0.05). siRNA knockdown partially reversed AE’s inhibition of NPC cell viability, proliferation, and migration. In vivo, AE attenuated tumor growth (p < 0.05), correlating with lncRNA D63785 downregulation and PI3K/Akt/mTOR dephosphorylation.

AE exerts anti-NPC effects by targeting the lncRNA D63785-PI3K/Akt/mTOR axis, offering a novel therapeutic strategy. These findings bridge AE’s pharmacological activity with lncRNA regulatory networks in NPC pathogenesis.