Evidence map›Paper›PMID 42824075›Full record

ArticleiScience2026

Mechanistic insights into VSIR-mediated AXL regulation and gastric cancer proliferation.

Jinshan Liu, Guoquan Huang, Yi Li, Yong Tan, Bo Qin, Changjiang Hao, Jilv Peng, Hongyang Zhu, Bitao Zhang, Yong Cheng and 1 more

Abstract read
In one paragraph

Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

11 authors.

Jinshan LiuDepartment of Gastrointestinal Surgery, the First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
Guoquan HuangHubei Key Laboratory for Translational Research in Traditional Chinese Medicine, Hubei Selenium and Human Health Institute, Department of Colorectal and Anal Surgery, The Central Hospital of Enshi Tujia and Miao Autonomous Prefecture, Hubei Minzu University, Enshi 445000, China.
Yi LiDepartment of Hepatobiliary Surgery, The Central Hospital of Enshi Tujia and Miao Autonomous Prefecture, Enshi 445000, China.
Yong TanState Key Laboratory of Biocatalysis and Enzyme Engineering, Hubei Key Laboratory of Industrial Biotechnology, School of Life Sciences, Hubei University, #368 Youyi Road, Wuhan 430062, P.R. China.
Bo QinHubei Key Laboratory for Translational Research in Traditional Chinese Medicine, Hubei Selenium and Human Health Institute, Department of Colorectal and Anal Surgery, The Central Hospital of Enshi Tujia and Miao Autonomous Prefecture, Hubei Minzu University, Enshi 445000, China.
Changjiang HaoHubei Key Laboratory for Translational Research in Traditional Chinese Medicine, Hubei Selenium and Human Health Institute, Department of Colorectal and Anal Surgery, The Central Hospital of Enshi Tujia and Miao Autonomous Prefecture, Hubei Minzu University, Enshi 445000, China.
Jilv PengHubei Key Laboratory for Translational Research in Traditional Chinese Medicine, Hubei Selenium and Human Health Institute, Department of Colorectal and Anal Surgery, The Central Hospital of Enshi Tujia and Miao Autonomous Prefecture, Hubei Minzu University, Enshi 445000, China.
Hongyang ZhuDepartment of General Surgery, Chongqing Hospital of Jiangsu Province Hospital, The People's Hospital of Qijiang District, Chongqing 401420, China.
Bitao ZhangHubei Key Laboratory for Translational Research in Traditional Chinese Medicine, Hubei Selenium and Human Health Institute, Department of Colorectal and Anal Surgery, The Central Hospital of Enshi Tujia and Miao Autonomous Prefecture, Hubei Minzu University, Enshi 445000, China.
Yong ChengDepartment of Gastrointestinal Surgery, the First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
Kun QianDepartment of Gastrointestinal Surgery, the First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gastric cancer (GC) progression is frequently driven by complex tumor microenvironment signals. Here, our study identifies V-set immunoregulatory receptor (VSIR) as a key driver of GC progression via AXL regulation. High-throughput RNA sequencing demonstrated that VSIR overexpression potently induces AXL upregulation in response to lipopolysaccharide (LPS) stimulation. This finding was confirmed through both VSIR overexpression and knockdown experiments. Mechanistically, our data demonstrated that STAT3 directly contributes to AXL transcriptional upregulation. Crucially, VSIR not only enhances LPS induced STAT3 phosphorylation, thereby amplifying AXL transcription, but also interacts with the AXL protein to stabilize it, leading to sustained AXL signaling. Functionally, the VSIR-AXL axis drives GC proliferation; notably, AXL inhibition suppresses this tumorigenesis, while combined AXL and HER2 blockade synergistically abrogates tumor growth. These findings reveal a critical oncogenic pathway and provide a strong rationale for dual-targeted therapeutic strategies in GC management.

Indexed as

AXLcombination therapygastric cancerHER2STAT3VSIR

Identifiers

PMID42824075
PMCPMC13626921

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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.