Evidence map›Paper›PMID 40604818›Full record

ArticleMolecular cancer2025

STK3 is a transcriptional target of YAP1 and a hub component in the crosstalk between Hippo and Wnt signaling pathways during gastric carcinogenesis.

Fuda Xie, Yang Lyu, Bonan Chen, Hoi Wing Leung, Peiyao Yu, Tiejun Feng, Canbin Fang, Alvin H K Cheung, Bin Zhou, Jianhui Jiang and 18 more

Abstract read
In one paragraph

Article in Molecular cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

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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

14 citing papers in PubMed.

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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

28 authors.

Fuda XieDepartment of Anatomical and Cellular Pathology, State Key Laboratory of Translational Oncology, Prince of Wales Hospital, Sir Y.K. Pao Cancer Center, The Chinese University of Hong Kong, Hong Kong, China.
Yang LyuDepartment of Anatomical and Cellular Pathology, State Key Laboratory of Translational Oncology, Prince of Wales Hospital, Sir Y.K. Pao Cancer Center, The Chinese University of Hong Kong, Hong Kong, China.
Bonan ChenDepartment of Anatomical and Cellular Pathology, State Key Laboratory of Translational Oncology, Prince of Wales Hospital, Sir Y.K. Pao Cancer Center, The Chinese University of Hong Kong, Hong Kong, China.
Hoi Wing LeungDepartment of Anatomical and Cellular Pathology, State Key Laboratory of Translational Oncology, Prince of Wales Hospital, Sir Y.K. Pao Cancer Center, The Chinese University of Hong Kong, Hong Kong, China.
Peiyao YuDepartment of Anatomical and Cellular Pathology, State Key Laboratory of Translational Oncology, Prince of Wales Hospital, Sir Y.K. Pao Cancer Center, The Chinese University of Hong Kong, Hong Kong, China.
Tiejun FengDepartment of Anatomical and Cellular Pathology, State Key Laboratory of Translational Oncology, Prince of Wales Hospital, Sir Y.K. Pao Cancer Center, The Chinese University of Hong Kong, Hong Kong, China.
Canbin FangDepartment of Anatomical and Cellular Pathology, State Key Laboratory of Translational Oncology, Prince of Wales Hospital, Sir Y.K. Pao Cancer Center, The Chinese University of Hong Kong, Hong Kong, China.
Alvin H K CheungDepartment of Anatomical and Cellular Pathology, State Key Laboratory of Translational Oncology, Prince of Wales Hospital, Sir Y.K. Pao Cancer Center, The Chinese University of Hong Kong, Hong Kong, China.
Bin ZhouDepartment of Anesthesiology, Renmin Hospital, Wuhan University, Wuhan, China.
Jianhui JiangGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Medical Research Center, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, China.
Ge ZhangLaw Sau Fai Institute for Advancing Translational Medicine in Bone and Joint Diseases (TMBJ), School of Chinese Medicine, Hong Kong Baptist University, Hong Kong, China.
Dazhi XuDepartment of Gastric Surgery, Department of Oncology, Shanghai Medical College, Fudan University Shanghai Cancer Center, Fudan University, Shanghai, China.
Liang LiDepartment of Pathology, Guangdong Province Key Laboratory of Molecular Tumor Pathology, Nanfang Hospital and Basic Medical College, Southern Medical University, Guangzhou, China.
Chen JiangDepartment of Pathology, State Key Laboratory of Oncology in South China, Guangdong Provincial Clinical Research Center for Cancer, Sun Yat- Sen University Cancer Center, Guangzhou, China.
Jianwu ChenDepartment of Burn and Plastic Surgery, General Hospital of Southern Theater Command, PLA, Guangzhou, China.
Zhaocai ZhouState Key Laboratory of Genetic Engineering, School of Life Sciences, Zhongshan Hospital, Fudan University, Shanghai, China.
Liwei AnDepartment of Stomatology, Department of Biochemistry and Molecular Biology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China.
Bing HuangGuangdong Provincial Key Laboratory of Gastroenterology, Department of Gastroenterology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Kangmin ZhuangGuangdong Provincial Key Laboratory of Gastroenterology, Department of Gastroenterology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Xiaobei LuoGuangdong Provincial Key Laboratory of Gastroenterology, Department of Gastroenterology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Kam Tong LeungDepartment of Pediatrics, The Chinese University of Hong Kong, Hong Kong, China.
Ching Hei ToDepartment of Clinical Oncology, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, China.
Brigette By MaDepartment of Clinical Oncology, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong, China.
Chi Chun WongInstitute of Digestive Disease, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Science, The Chinese University of Hong Kong, Hong Kong, China.
William Kk WuDepartment of Anaesthesia and Intensive Care, The Chinese University of Hong Kong, Hong Kong, China.
Jun YuInstitute of Digestive Disease, State Key Laboratory of Digestive Disease, Li Ka Shing Institute of Health Science, The Chinese University of Hong Kong, Hong Kong, China.
Ka Fai ToDepartment of Anatomical and Cellular Pathology, State Key Laboratory of Translational Oncology, Prince of Wales Hospital, Sir Y.K. Pao Cancer Center, The Chinese University of Hong Kong, Hong Kong, China.
Wei KangDepartment of Anatomical and Cellular Pathology, State Key Laboratory of Translational Oncology, Prince of Wales Hospital, Sir Y.K. Pao Cancer Center, The Chinese University of Hong Kong, Hong Kong, China. weikang@cuhk.edu.hk.

Funding

Basic and Applied Basic Research Foundation of Guangdong Province 2022A1515011477CUHK direct research grant 2024.066National Natural Science Foundation of China 82272990National Natural Science Foundation of China 82303855NSFC-RGC Joint Research Scheme N_CUHK448/23
6 · The paper itself

Abstract

backgroundSerine/threonine kinase 3 (STK3) is recognized as a key regulator in Hippo pathway and a tumor-suppressing gene in various cancer types. However, its non-canonical role has been gradually revealed in cancer development.

methodsOur objective is to elucidate the upregulation pattern and molecular mechanisms of STK3 in advancing gastric cancer (GC) progression. The regulation of YAP1 on STK3 was assessed through a combination of bulk and single-cell RNA-sequencing, Western blot, ChIP-qPCR, gene knockout mouse models, and functional rescue assays. The oncogenic roles of STK3 were confirmed through subcutaneous xenograft formation models and functional assays including spheroid formation and organoid growth. The phosphorylated target of STK3 was revealed by co-immunoprecipitation and in vitro kinase assays. STK3-targeted drugs were screened out by molecular docking and cellular thermal shift assay (CETSA).

resultsReduction of YAP1 significantly impaired STK3 expression at both mRNA and protein levels, and deletion of STK3 partially attenuated the oncogenic activity of YAP1. Notably, MNNG-induced tumors in Yap1

conclusionsSTK3 was identified as a transcriptional target of YAP1, leading to enhanced DNA repair ability and stemness acquisition during GC progression by activating Wnt/β-catenin activity through GSK-3β degradation. Moreover, STK3-targeted therapy offered a novel approach to concur acquired chemo-resistance in GC patients.

Indexed as

Adaptor Proteins, Signal TransducingGene Expression Regulation, NeoplasticProtein Serine-Threonine KinasesSerine-Threonine Kinase 3Stomach NeoplasmsTranscription FactorsWnt Signaling PathwayAnimalsCarcinogenesisCell Cycle ProteinsCell Line, TumorCell ProliferationHippo KinasesHippo Signaling PathwayHumansMiceAdaptor Proteins, Signal TransducingCell Cycle ProteinsHippo KinasesProtein Serine-Threonine KinasesSerine-Threonine Kinase 3STK3 protein, humanTranscription FactorsYAP1 protein, humanYap1 protein, mouseYAP-Signaling ProteinsGastric cancerSTK3Wnt signalingYAP1

Identifiers

PMID40604818
PMCPMC12220525

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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.