Evidence map›Paper›PMID 41975153›Full record

ArticleBlood research2026

Targeting the HERV-K102 envelope elicits pyroptosis and represents a novel therapeutic strategy for acute myeloid leukemia.

Lihong Zong, Qian Luo, Jingru Zhao, Huyi Lei, Hui Liu, Mengyuan Li, Yiyuan Chen, Minghuan Zhang, Rongzhen Xu, Wenbin Qian

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Blood research, 2026. 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. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors.

Lihong Zong *Department of Hematology, The Second Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
Qian Luo *Department of Hematology, The Second Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
Jingru Zhao *Department of Hematology, The Second Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
Huyi LeiDepartment of Hematology, The Affiliated Hospital of ShaoXing University (ShaoXing Municipal Hospital), Shaoxing, Zhejiang, China.
Hui LiuDepartment of Hematology, The Second Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
Mengyuan LiDepartment of Hematology, The Second Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
Yiyuan ChenDepartment of Hematology, The Second Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
Minghuan ZhangDepartment of Hematology, The Second Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.
Rongzhen XuDepartment of Hematology, The Second Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, China. zrxyk10@zju.edu.cn.
Wenbin QianDepartment of Hematology, The Second Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang, China. qianwb@zju.edu.cn.

Funding

the National Natural Science Foundation of China No. 82400217Zhejiang Provincial Natural Science Foundation of China No. LBY24H080003
6 · The paper itself

Abstract

objectiveSeveral recent studies have focused on human endogenous retroviruses (HERVs). HERVs entered the human genome millions of years ago and are associated with various diseases including cancer and immune regulation. Among these, the HERV-K family exhibits the highest transcriptional activity. However, little is known about the expression of HERVs in acute myeloid leukemia (AML) and their potential as biomarkers or therapeutic targets. This study primarily investigated the role of HERV-K102 in AML development and explored the underlying mechanisms.

methodsThe expression profiles of HERV K102 in AML and normal samples were analyzed using The Cancer Genome Atlas (TCGA) database and AML cell lines. Knockout models were generated using CRISPR-Cas9-mediated deletion of the HERV-K102 envelope (K-Env). Cell viability and pyroptosis rates were measured using the MTT assay and flow cytometry, respectively. Transcriptome analysis was performed to identify differentially expressed genes and related pathways. Pyroptosis markers were detected using qRT-PCR and western blotting. The role of HERV-K102 in AML was validated using an inducible knockout xenograft tumor model.

resultsHERV-K102 was aberrantly activated and highly expressed in AML cells. K-Env depletion inhibited AML cell proliferation and promoted apoptosis. Furthermore, K-Env knockout induced pyroptosis, as indicated by increased lactate dehydrogenase (LDH) release and enhanced cleavage of caspase-1 and gasdermin D (GSDMD). Transcriptomic and functional analyses demonstrated that this process is mediated by S100A9 upregulation and activation of the NOD-like receptor protein 3 (NLRP3) inflammasome pathway.

conclusionOur findings suggest that HERV-K102 Env may play an important role in AML pathogenesis and represents a novel diagnostic and therapeutic target.

Indexed as

AMLHERV-102Pyroptosis

Identifiers

PMID41975153
PMCPMC13184007

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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.