Evidence map›Paper›PMID 41162883›Full record

ArticleMolecular medicine (Cambridge, Mass.)2025

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

Shengquan Liu, Shaoxiong Wang, Yahong Xu, Yuanling Huang, Pengliang Xin, Yan Zheng, Yishen Wu, Yanling Yang, Xiongpeng Zhu, Chuntuan Li

Abstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Total Flavonoids fromInternational journal of molecular sciences · 2026
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Shengquan LiuDepartment of Hematology, First Hospital of Quanzhou Affiliated to Fujian Medical University, 248 East Street, Licheng District, Quanzhou, 362000, Fujian Province, China.
Shaoxiong WangDepartment of Hematology, First Hospital of Quanzhou Affiliated to Fujian Medical University, 248 East Street, Licheng District, Quanzhou, 362000, Fujian Province, China.
Yahong XuDepartment of Hematology, First Hospital of Quanzhou Affiliated to Fujian Medical University, 248 East Street, Licheng District, Quanzhou, 362000, Fujian Province, China.
Yuanling HuangDepartment of Hematology, First Hospital of Quanzhou Affiliated to Fujian Medical University, 248 East Street, Licheng District, Quanzhou, 362000, Fujian Province, China.
Pengliang XinDepartment of Hematology, First Hospital of Quanzhou Affiliated to Fujian Medical University, 248 East Street, Licheng District, Quanzhou, 362000, Fujian Province, China.
Yan ZhengDepartment of Hematology, First Hospital of Quanzhou Affiliated to Fujian Medical University, 248 East Street, Licheng District, Quanzhou, 362000, Fujian Province, China.
Yishen WuDepartment of Hematology, First Hospital of Quanzhou Affiliated to Fujian Medical University, 248 East Street, Licheng District, Quanzhou, 362000, Fujian Province, China.
Yanling YangDepartment of Hematology, First Hospital of Quanzhou Affiliated to Fujian Medical University, 248 East Street, Licheng District, Quanzhou, 362000, Fujian Province, China.
Xiongpeng ZhuDepartment of Hematology, First Hospital of Quanzhou Affiliated to Fujian Medical University, 248 East Street, Licheng District, Quanzhou, 362000, Fujian Province, China. xiongpengzhu@163.com.
Chuntuan LiDepartment of Hematology, First Hospital of Quanzhou Affiliated to Fujian Medical University, 248 East Street, Licheng District, Quanzhou, 362000, Fujian Province, China. lct090909@163.com.

Funding

Fujian Provincial Natural Science Foundation of China 2023J011770
6 · The paper itself

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.

Indexed as

ApoptosisGene SilencingLymphoma, T-CellSmoothened ReceptorAnimalsB7-H1 AntigenCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansMiceRNA InterferenceXenograft Model Antitumor AssaysB7-H1 AntigenSmoothened ReceptorSMO protein, humanCell apoptosisCell proliferationGene therapyNatural Killer/T-Cell lymphomaSmo silencingXenotransplantation

Identifiers

PMID41162883
PMCPMC12574012

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.