Evidence map›Paper›PMID 42361687›Full record

ArticleTranslational oncology2026

S100A10 promotes tumorigenesis and metastasis in lung adenocarcinoma by regulating JUND/TNC axis-mediated EMT.

Zhixin Zheng, Anjie Peng, Ziyao Xi, Haibin Ou, Jiong Liu, Aoqing Ye, Jing Shao, Feng Li, Yu Liu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

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

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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2 · The registry

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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

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5 · Who and what money

Authors and funding

9 authors.

Zhixin ZhengDepartment of Radiation and Medical Oncology, Hubei Key Laboratory of Tumor Biological Behaviors, Hubei Province Cancer Clinical Study Center, Zhongnan Hospital, Wuhan University, Wuhan, Hubei, China. Electronic address: 2018305230075@whu.edu.cn.
Anjie PengDepartment of Radiation and Medical Oncology, Hubei Key Laboratory of Tumor Biological Behaviors, Hubei Province Cancer Clinical Study Center, Zhongnan Hospital, Wuhan University, Wuhan, Hubei, China. Electronic address: penganjie@whu.edu.cn.
Ziyao XiShanghai Public Health Clinical Center, Fudan University, Shanghai, China. Electronic address: 15515807065@163.com.
Haibin OuDepartment of Radiation and Medical Oncology, Hubei Key Laboratory of Tumor Biological Behaviors, Hubei Province Cancer Clinical Study Center, Zhongnan Hospital, Wuhan University, Wuhan, Hubei, China. Electronic address: 2010302180151@whu.edu.cn.
Jiong LiuDepartment of Radiation and Medical Oncology, Hubei Key Laboratory of Tumor Biological Behaviors, Hubei Province Cancer Clinical Study Center, Zhongnan Hospital, Wuhan University, Wuhan, Hubei, China. Electronic address: 2018305231150@whu.edu.cn.
Aoqing YeDepartment of Radiation and Medical Oncology, Hubei Key Laboratory of Tumor Biological Behaviors, Hubei Province Cancer Clinical Study Center, Zhongnan Hospital, Wuhan University, Wuhan, Hubei, China. Electronic address: aoqing_ye@163.com.
Jing ShaoNo. 1 Zhifang Culture Avenue, Jiangxia District, Wuhan Jiangxia District First People's Hospital, Wuhan, Hubei, China. Electronic address: shaojing@whu.edu.cn.
Feng LiKey Laboratory of Biomedical Polymers of Ministry of Education, College of Chemistry and Molecular Science, Wuhan University, Wuhan, Hubei, China. Electronic address: fli222@whu.edu.cn.
Yu LiuDepartment of Radiation and Medical Oncology, Hubei Key Laboratory of Tumor Biological Behaviors, Hubei Province Cancer Clinical Study Center, Zhongnan Hospital, Wuhan University, Wuhan, Hubei, China. Electronic address: liuyu97@whu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRecurrence and metastasis significantly impact the prognosis of lung adenocarcinoma (LUAD), yet effective therapies targeting these processes remain limited, especially in advanced stages. This study investigates the role of S100A10 as an oncogenic driver in LUAD progression via epithelial-mesenchymal transition (EMT).

methodsS100A10 expression was analyzed in public datasets and correlated with patient survival. Functional studies involved S100A10 knockdown or overexpression in LUAD cell lines, assessing viability (CCK-8), migration, invasion (Transwell, wound healing), mRNA (qPCR), and protein (Western blot). Tumorigenicity was evaluated using in vivo models. A small-molecule inhibitor, [D-Leu-4]-OB3, was identified through virtual screening and tested for its effect on S100A10 and LUAD.

resultsHigh S100A10 expression correlated with poor outcomes in LUAD. Knockdown of S100A10 suppressed cell viability, migration, invasion, and EMT both in vitro and in vivo, while overexpression enhanced these malignant traits. Mechanistically, S100A10 activated JUND and Tenascin-C (TNC), promoting EMT. Re-expression of TNC rescued the anti-metastatic effects of S100A10 inhibition. [D-Leu-4]-OB3 specifically targeted S100A10, inhibiting LUAD growth and metastasis.

conclusionS100A10 promotes LUAD progression and metastasis through JUND/TNC-mediated EMT. [D-Leu-4]-OB3 represents a promising targeted therapy for LUAD by inhibiting S100A10.

Indexed as

EMTJUND/TNC axisLUADS100a10

Identifiers

PMID42361687
PMCPMC13324493

What Socratic holds

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LicenceCC BY-NC-ND
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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 Socratic graph.