Evidence map›Paper›PMID 41937564›Full record

ArticleActa biochimica et biophysica Sinica2026

MerTK inhibition by UNC569 triggers DNA damage and JNK/p38 MAPK cascade-driven apoptosis in pancreatic cancer.

Meng Guo, Junwan Lu, Yue Sun, Lan Wang, Wen Li, Peizhen Wang, Yao Deng, Zhijie Tan, Hanbin Chen, Yang Hu and 2 more

Abstract read
In one paragraph

Article in Acta biochimica et biophysica Sinica, 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

12 authors.

Meng GuoMOE Key Lab of Rare Pediatric Diseases, Department of Cell Biology and Genetics, School of Basic Medical Sciences, Hengyang Medical School, University of South China, Hengyang 421001, China.
Junwan LuMedical Molecular Biology Laboratory, School of Medicine, Jinhua University of Vocational Technology, Jinhua 321016, China.
Yue SunDepartment of Ultrasound, The Affiliated Hospital of Yunnan University, Kunming 650021, China.
Lan WangMedical Molecular Biology Laboratory, School of Medicine, Jinhua University of Vocational Technology, Jinhua 321016, China.
Wen LiDepartment of Pathology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325035, China.
Peizhen WangDepartment of Pathology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325035, China.
Yao DengMOE Key Lab of Rare Pediatric Diseases, Department of Cell Biology and Genetics, School of Basic Medical Sciences, Hengyang Medical School, University of South China, Hengyang 421001, China.
Zhijie TanMOE Key Lab of Rare Pediatric Diseases, Department of Cell Biology and Genetics, School of Basic Medical Sciences, Hengyang Medical School, University of South China, Hengyang 421001, China.
Hanbin ChenDepartment of Oncology, The First Affiliated Hospital, Wenzhou Medical University, Wenzhou 325000, China.
Yang HuDepartment of Gastroenterology, The Affiliated Nanhua Hospital, Hengyang Medical School, University of South China, Hengyang 421001, China.
Bin LuMOE Key Lab of Rare Pediatric Diseases, Department of Cell Biology and Genetics, School of Basic Medical Sciences, Hengyang Medical School, University of South China, Hengyang 421001, China.
Rongrong WangDepartment of Pathology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325035, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is a malignancy with increasing mortality rates and remains a major clinical challenge due to its aggressive progression and limited therapeutic options. Therefore, the identification of early biomarkers and the development of effective targeted therapies are critically needed. MerTK, a receptor tyrosine kinase aberrantly expressed in various cancers, can be selectively inhibited by UNC569, a small-molecule antagonist with demonstrated efficacy in hematologic malignancies. This study shows that UNC569 potently suppresses PDAC cell proliferation and clonogenic growth, inhibits migration and invasion by attenuating epithelial-mesenchymal transition, and enhances the sensitivity of PDAC cells to Gemcitabine while promoting apoptosis. Mechanistically, UNC569 induces DNA damage-mediated G2/M phase arrest and activates JNK/p38 mitogen-activated protein kinase-dependent apoptotic signaling. Collectively, these results establish MerTK as a promising therapeutic target in PDAC and highlight the translational potential of UNC569 as a dual-pathway inhibitor for PDAC treatment.

Indexed as

ApoptosisCarcinoma, Pancreatic Ductalc-Mer Tyrosine KinaseDNA DamageMAP Kinase Signaling SystemPancreatic NeoplasmsProtein Kinase InhibitorsCell Line, TumorCell MovementCell ProliferationDeoxycytidineEpithelial-Mesenchymal TransitionGemcitabineHumansp38 Mitogen-Activated Protein KinasesThiophenes3-(carbamoylamino)-5-(3-fluorophenyl)-N-(3-piperidyl)thiophene-2-carboxamidec-Mer Tyrosine KinaseDeoxycytidineGemcitabineMERTK protein, humanp38 Mitogen-Activated Protein KinasesProtein Kinase InhibitorsThiophenesUreaDNA damageJNK/p38 MAPKMerTKpancreatic cancerUNC569

Identifiers

PMID41937564
PMCPMC13449087

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.