In one paragraphArticle in Cancer research, 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
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 registryThe 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 literatureWho cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
4 · The recordCorrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what moneyAuthors and funding
24 authors.
Xianglin Yin *Department of Pathology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.ORCID 0009-0006-3564-457X Xiao-Ding Liu *Department of Pathology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.ORCID 0000-0002-6233-3201 Lulu Cheng *Department of Pathology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.ORCID 0009-0004-5622-8845 Lin YangDepartment of Pathology, Institute of Basic Medical Sciences and School of Basic Medicine, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.ORCID 0000-0003-1898-8558 Yujie FuDepartment of Pathology, Institute of Basic Medical Sciences and School of Basic Medicine, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.ORCID 0000-0001-6139-0004 Yifan LiDepartment of Pathology, Institute of Basic Medical Sciences and School of Basic Medicine, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.ORCID 0009-0009-4126-7426 Mengqi ChangInstitute of Clinical Medicine, National Infrastructures for Translational Medicine, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.ORCID 0000-0002-9588-953X Lingfeng XiaoDepartment of Pathology, Institute of Basic Medical Sciences and School of Basic Medicine, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.ORCID 0000-0001-9004-2818 Zhenli YangCell Resource Center, Institute of Basic Medical Sciences and School of Basic Medicine, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.ORCID 0009-0000-8068-4067 Bohan LiuDepartment of Pathology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.ORCID 0000-0002-3298-7490 Jun WangDepartment of Pathology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.ORCID 0009-0006-9774-4293 Xuqing ShiDepartment of Pathology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.ORCID 0009-0008-9061-5442 Xinyi KeDepartment of Pathology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.ORCID 0009-0003-2228-3371 Qixian LiuDepartment of Pathology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.ORCID 0009-0002-8872-1891 Hangqi LiuDepartment of Pathology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.ORCID 0000-0001-8973-6943 Tianqi LiuDepartment of Pathology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.ORCID 0000-0002-3304-6203 Mu ZhangDepartment of Pathology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.ORCID 0009-0003-1080-6040 Yuhan ZhangDepartment of Pathology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.ORCID 0009-0001-3122-1290 Longyun ChenDepartment of Pathology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.ORCID 0000-0002-5895-7580 Junyi PangDepartment of Pathology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.ORCID 0000-0002-0785-811X Huanwen WuDepartment of Pathology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.ORCID 0000-0002-3996-3176 Wei-Min TongDepartment of Pathology, Institute of Basic Medical Sciences and School of Basic Medicine, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.ORCID 0000-0002-6240-0267 Yamei NiuDepartment of Pathology, Institute of Basic Medical Sciences and School of Basic Medicine, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.ORCID 0000-0003-2078-0780 Zhiyong LiangDepartment of Pathology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.ORCID 0000-0003-4787-2925 Funding
Chinese Academy of Medical Sciences (CAMS) 2021-I2M-1-002Fundamental Research Funds for the Central Universities (Fundamental Research Fund for the Central Universities) 3332024005National High Level Hospital Clinical Research Funding 2022-PUMCH-B-061National High Level Hospital Clinical Research Funding 2025-PUMCH-D-002National Key Clinical Specialty Construction Project U114000National Natural Science Foundation of China (NSFC) 82403474Natural Science Foundation of Beijing Municipality () 7252094
6 · The paper itselfAbstract
Cancer-associated fibroblasts (CAF) are principal determinants of pancreatic ductal adenocarcinoma (PDAC) progression. CAFs can shape tumor behavior via multiple pathways, underscoring the need for a complete understanding of the regulatory mechanisms that govern CAF function. In this study, we identified N6-methyladenosine (m6A) remodeling as a hallmark of CAF activation and defined a critical role for the m6A demethylase ALKBH5 in PDAC metastasis. Activated CAFs exhibited a global reduction in m6A abundance, with ALKBH5 emerging as a key regulator of the CAF epitranscriptome. Functionally, CAF-derived ALKBH5 enhanced pancreatic cancer cell migration and invasion in vitro and promoted epithelial-mesenchymal transition-associated gene expression in tumor cells in an m6A-dependent manner. Orthotopic co-implantation models and host genetic ablation models demonstrated that ALKBH5 plays a critical role in metastatic dissemination, with minimal impact on primary tumor growth. Mechanistically, ALKBH5 enhanced the m6A-dependent translation of HSF1 in CAFs, at least in part by relieving insulin-like growth factor 2 mRNA-binding protein 3-associated translational constraints. Elevated HSF1 subsequently activated leukemia-inhibitory factor (LIF) transcription through distal enhancer elements, establishing an ALKBH5-HSF1-LIF signaling axis that mediated the prometastatic CAF-tumor cell communication. Clinically, enrichment of ALKBH5+HSF1+ CAFs independently predicted poor prognosis and was preferentially observed in metastatic PDAC. Collectively, these findings uncover a CAF-intrinsic epitranscriptomic program that drives PDAC metastasis and highlight stromal m6A regulation as a potential therapeutic vulnerability. SIGNIFICANCE: Cancer-associated fibroblast-intrinsic ALKBH5 facilitates metastatic dissemination in pancreatic ductal adenocarcinoma via m6A-dependent HSF1-LIF paracrine signaling, uncovering a stroma-specific vulnerability with therapeutic relevance in pancreatic cancer.
Indexed as
AlkB Homolog 5, RNA DemethylaseCancer-Associated FibroblastsCarcinoma, Pancreatic DuctalPancreatic NeoplasmsAdenosineAnimalsCell Line, TumorCell MovementEpithelial-Mesenchymal TransitionEpitranscriptomeEpitranscriptomicsGene Expression Regulation, NeoplasticHumansMiceNeoplasm MetastasisRNA MethylationAdenosineALKBH5 protein, humanAlkB Homolog 5, RNA DemethylaseN-methyladenosine
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