# Smo gene silencing: a promising strategy for natural killer/t-cell lymphoma treatment via modulating proliferation and apoptosis

## TL;DR

This study shows that silencing the Smo gene can reduce the growth and increase the death of cancer cells in a type of lymphoma called NKTCL.

## Contribution

This is the first study to demonstrate the anti-tumor effects of Smo gene silencing in NKTCL cells.

## Key findings

- Smo gene silencing significantly inhibited the proliferation of NKTCL cells.
- Smo silencing increased apoptosis rates in NKTCL cells.
- Smo silencing reduced the expression of Gli1 and PD-L1 in NKTCL cells.

## Abstract

Natural killer/T-cell lymphoma (NKTCL) is a malignancy with a poor prognosis. The Smoothened (Smo) protein is implicated in NKTCL growth. This study employed lentiviral vector-mediated Smo RNA interference (LV-Smo-RNAi) to silence the Smo gene in the human NKTCL cell line SNT8. Fluorescence microscopy, qRT-PCR, and Western blot verified the reduction of Smo mRNA and protein levels. The CCK-8 assay showed that Smo silencing inhibited cell proliferation. Flow cytometry with annexin V-PE/7-AAD double staining indicated an increased apoptosis rate. Moreover, the expression of GLI family zinc finger 1 (Gli1) and programmed death-ligand 1 (PD-L1) was downregulated. In vivo, xenotransplantation experiments demonstrated that Smo silencing led to slower tumor growth with reduced tumor volume and weight. Overall, Smo gene silencing holds great potential as a novel molecular-targeted therapy approach for NKTCL by effectively suppressing cell proliferation and promoting apoptosis.

The online version contains supplementary material available at 10.1186/s10020-025-01341-z.

1. This study is the first to report the anti-tumor effects of Smo gene silencing in the human NKTCL cell line SNT8

2. This research finds that Smo gene silencing significantly suppresses cell proliferation.

3. This research observes that Smo silencing significantly increases the apoptosis rate of NKTCL cells.

4. Smo silencing downregulates the expression of Gli1 and PD-L1, providing new insights into the underlying mechanisms.

5.This study provides a new molecular target for developing targeted therapies for NKTCL.

The online version contains supplementary material available at 10.1186/s10020-025-01341-z.