Evidence map›Paper›PMID 42092950›Full record

ArticleJournal of experimental & clinical cancer research : CR2026

Klf4-Tymp axis promotes inflammation-driven early tumorigenesis by enhancing kras mutation-induced acinar-to-ductal metaplasia through Pi3k/Akt and Mek/Erk pathways.

Qihang Yuan, Junhong Chen, Peng Luo, Kai Liu, Fangyue Guo, Yao Xu, Mengying Tong, Hong Xiang, Dong Shang

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Article in Journal of experimental & clinical cancer research : CR, 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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5 · Who and what money

Authors and funding

9 authors.

Qihang Yuan *Pancreas and Biliary Center, Department of General Surgery, First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning, China.
Junhong Chen *Department of Hepatobiliary and Pancreatic Surgery, General Surgery Center, First Hospital of Jilin University, Changchun, Jilin, China.
Peng Luo *Department of Oncology, Zhujiang Hospital, Southern Medical University, Guangzhou, China.
Kai LiuDepartment of Hepatobiliary and Pancreatic Surgery, General Surgery Center, First Hospital of Jilin University, Changchun, Jilin, China.
Fangyue GuoClinical Laboratory of Integrative Medicine, First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning, China.
Yao XuClinical Laboratory of Integrative Medicine, First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning, China.
Mengying TongDepartment of Ultrasound, First Affiliated Hospital of Dalian Medical University, Dalian, China. mengyingtong@dmu.edu.cn.
Hong XiangClinical Laboratory of Integrative Medicine, First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning, China. xianghong@dmu.edu.cn.
Dong ShangPancreas and Biliary Center, Department of General Surgery, First Affiliated Hospital of Dalian Medical University, Dalian, Liaoning, China. shangdongdalian@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAcinar-to-ductal metaplasia (ADM) is a pivotal step in pancreatic tumorigenesis, reversible in normal contexts but progressing to PanIN and pancreatic cancer (PC) in the presence of Kras mutation and inflammation. Thus, delineating exocrine cell heterogeneity and identifying regulators of ADM are essential for understanding pancreatic tumorigenesis.

methodsWe collected single-cell RNA sequencing (scRNA-seq) data of 146 human pancreatic samples, followed by comprehensive exploration of dynamic change and heterogeneity of ADM via machine learning algorithms. Multi-omics analysis integrating ATAC-seq and RNA-seq highlights the association of Klf4-Tymp axis with ADM. A dual-luciferase reporter assay was performed to evaluate the transcriptional activation of the Tymp promoter by Klf4. AAV-mediated gene silencing was performed in vivo to elucidate the roles and underlying mechanisms of the Klf4/Tymp axis during the ADM process in Pdx1-Cre; Kras

resultsscRNA-seq revealed one S100A4

conclusionsThe Klf4-Tymp axis promotes inflammation-associated early pancreatic tumorigenesis by enhancing KRAS mutation-induced ADM through activation of the Pi3k/Akt and Mek/Erk signaling pathways. These findings provide new insights into the molecular mechanisms linking inflammatory injury to ADM and early pancreatic tumorigenesis.

Indexed as

InflammationKruppel-Like Transcription FactorsPancreatic NeoplasmsProto-Oncogene Proteins p21(ras)Acinar CellsAnimalsCarcinogenesisHumansKruppel-Like Factor 4MAP Kinase Signaling SystemMetaplasiaMiceMutationPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktKLF4 protein, humanKlf4 protein, mouseKRAS protein, humanKruppel-Like Factor 4Kruppel-Like Transcription FactorsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktProto-Oncogene Proteins p21(ras)Acinar-to-Ductal MetaplasiaInflammationKLF4Pancreatic TumorigenesisScRNA-seqTYMP

Identifiers

PMID42092950
PMCPMC13474847

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