Evidence map›Paper›PMID 42778663›Full record

ArticleOncogene2026

DDR1 sustains ferroptosis resistance in pancreatic ductal adenocarcinoma via SLC40A1-mediated iron homeostasis.

Chao Song, Luting Zhang, Sheng Xu, Xu-An Wang, Xinyi Zhang, Kai Xuan Cheong, Ganggang Wang, Mengmeng Liu, Yazhou Wang, Yifei Zhang and 10 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 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

20 authors.

Chao Song *Department of Pancreatic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
Luting Zhang *Department of Pancreatic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
Sheng Xu *Shanghai Institute of Nutrition and Health, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, China.ORCID http://orcid.org/0009-0006-4430-9378
Xu-An Wang *Department of Pancreatic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
Xinyi ZhangDepartment of Pancreatic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
Kai Xuan CheongDepartment of Pancreatic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
Ganggang WangDepartment of Liver Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
Mengmeng LiuDepartment of Gastroenterology Surgery, Qingpu Branch, Affiliated Zhongshan Hospital of Fudan University, Shanghai, China.
Yazhou WangDepartment of Pancreatic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
Yifei ZhangDepartment of Pancreatic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
Taochen HeDepartment of Pancreatic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China.
Kai DingShanghai Institute of Nutrition and Health, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, China.
Yu ChenShanghai Institute of Nutrition and Health, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, China.
Xin LiangShanghai Institute of Nutrition and Health, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, China.
Bing ZhuShanghai Institute of Nutrition and Health, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, China.ORCID http://orcid.org/0009-0001-7162-7420
Qianzhi NiShanghai Institute of Nutrition and Health, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, China.
Wenquan WangDepartment of Pancreatic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China. wang.wenquan@zs-hospital.sh.cn.ORCID http://orcid.org/0000-0002-4696-8098
Jingjing LiShanghai Institute of Nutrition and Health, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, China. tide7@163.com.ORCID http://orcid.org/0000-0002-3973-5405
Wenhui LouDepartment of Pancreatic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China. lou.wenhui@zs-hospital.sh.cn.ORCID http://orcid.org/0000-0001-5820-6843
Liang LiuDepartment of Pancreatic Surgery, Zhongshan Hospital, Fudan University, Shanghai, China. liu.liang@zs-hospital.sh.cn.ORCID http://orcid.org/0009-0002-0403-6580

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Integrated single-cell transcriptomics and clinical analyses reveal elevated DDR1 expression in pancreatic ductal adenocarcinoma (PDAC) tissues, which correlates with poor prognosis. Mechanistically, collagen-activated Discoidin Domain Receptor 1 (DDR1) recruits SHC1 to activate the MAPK/ERK pathway, thereby driving transcriptional upregulation of SLC40A1 via the ERK-MYC axis. SLC40A1, encoding an iron exporter, reduces intracellular labile iron pools, thereby suppressing lipid peroxidation and ferroptosis. Consequently, DDR1 overexpression confers resistance to dihydroartemisinin (DHA)-induced ferroptosis in PDAC cells, characterized by diminished ROS accumulation, mitochondrial shrinkage, and cristae loss. Conversely, DDR1 knockdown or pharmacological inhibition (Dasatinib) sensitizes PDAC cells to DHA. Crucially, combining Dasatinib and DHA treatment synergistically inhibits tumor growth in vivo by reactivating ferroptosis, as evidenced by increased 4-HNE accumulation and decreased Ki67 expression. These findings identify DDR1 as a key regulator of iron metabolism and ferroptosis in PDAC, suggesting that dual targeting of DDR1 and ferroptosis represents a promising therapeutic strategy.

Identifiers

PMID42778663

What OpenQuestion holds

Textmetadata
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.