Evidence map›Paper›PMID 40874680›Full record

ArticleCancer medicine2025

MCPIP1 Controls Hybrid EMT and Tumor Stemness via the IL6/JAK2/STAT3 Axis in Pancreatic Cancer.

Xihui Ding, Yingying Zheng, Min Liu, Fu Lai, Shiqi Liu, Qiuping Chen, Zihao Zhu, Huanzhong Liu, Xiaohui Li, Jinyong Xu and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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.

Xihui DingDepartment of Anatomy, Anhui Medical University, Hefei, Anhui, China.ORCID https://orcid.org/0009-0005-9285-2095
Yingying ZhengDepartment of Anatomy, Anhui Medical University, Hefei, Anhui, China.
Min LiuDepartment of Anatomy, Anhui Medical University, Hefei, Anhui, China.
Fu LaiDepartment of Anatomy, Anhui Medical University, Hefei, Anhui, China.
Shiqi LiuDepartment of Anatomy, Anhui Medical University, Hefei, Anhui, China.
Qiuping ChenDepartment of Anatomy, Anhui Medical University, Hefei, Anhui, China.
Zihao ZhuSecond Clinical Medical College, Anhui Medical University, Hefei, Anhui, China.
Huanzhong LiuDepartment of Psychiatry, Chaohu Hospital of Anhui Medical University, Hefei, Anhui, China.
Xiaohui LiDepartment of Anatomy, Anhui Medical University, Hefei, Anhui, China.
Jinyong XuDepartment of Anatomy, Anhui Medical University, Hefei, Anhui, China.
Rui WangDepartment of Anatomy, Anhui Medical University, Hefei, Anhui, China.
Zhenhua RenDepartment of Anatomy, Anhui Medical University, Hefei, Anhui, China.ORCID https://orcid.org/0000-0002-1426-7457

Funding

Major Projects of the Ministry of Science and Technology of China 2021ZD0201102Major Projects of the Ministry of Science and Technology of China 2023YFA1800802the National Natural Science Foundation of China 82071401
6 · The paper itself

Abstract

introductionPancreatic cancer (PC) is a common malignant tumor with high morbidity and mortality and a very poor prognosis, highlighting the urgent need to identify molecular therapeutic targets. Monocyte chemotactic protein-inducible protein-1 (MCPIP1) is a common inflammatory protein associated with the pathogenesis of a variety of cancers, although a comprehensive understanding of its function and the underlying mechanisms involved in PC remains unclear. MATERIALS AND

methodsImmunohistochemistry, western blotting, immunofluorescence, flow cytometry, Transwell, and the scratch assay were used to evaluate the functional role of MCPIP1 in PC. Human PC samples, PC cells, and tumor tissues from subcutaneous tumors of nude mice were examined for MCPIP1 and a panel of epithelial-mesenchymal transition (EMT) -related indicators. In the mechanistic study, the IL6/JAK/STAT3 signaling pathway was investigated as a potential downstream pathway. IL6 activity was inhibited using the pharmacological inhibitor LMT-28 and was applied to MCPIP1 gene-deficient cells to assess the reversal of the malignant phenotype.

resultsMCPIP1 was significantly downregulated in PC tissues and its expression strongly correlated with patient survival. MCPIP1 knockdown enhanced tumor cell stemness, proliferation, migration, and hybrid epithelial-mesenchymal transition (hybrid EMT) in PC cell lines, whereas overexpression suppressed these phenotypes. In xenograft models, MCPIP1 knockdown promoted tumor growth and hybrid EMT progression in mice. MCPIP1 knockdown activated the IL6/JAK/STAT3 signaling pathway, which was inhibited by MCPIP1 overexpression. LMT-28 treatment reversed the stemness and hybrid EMT phenotypes of MCPIP1-deficient cells.

conclusionMCPIP1 is a key regulator of PC progression, acting as a tumor suppressor by inhibiting the IL6/JAK/STAT3 signaling pathway. The findings suggest that MCPIP1 is a promising therapeutic target with potential implications for the development of new strategies for managing PC.

Indexed as

Epithelial-Mesenchymal TransitionInterleukin-6Janus Kinase 2Neoplastic Stem CellsPancreatic NeoplasmsRibonucleasesSTAT3 Transcription FactorTranscription FactorsAnimalsCell Line, TumorCell MovementCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansMaleIL6 protein, humanInterleukin-6JAK2 protein, humanJanus Kinase 2RibonucleasesSTAT3 protein, humanSTAT3 Transcription FactorTranscription FactorsZC3H12A protein, humanhybrid epithelial‐mesenchymal transitionIL6/JAK/STAT3 axismonocyte chemotactic protein‐inducible protein‐1pancreatic cancertumor stemness

Identifiers

PMID40874680
PMCPMC12392288

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.