Evidence map›Paper›PMID 39792573›Full record

ArticleMolecular oncology2025

Cystatin A promotes the antitumor activity of T helper type 1 cells and dendritic cells in murine models of pancreatic cancer.

Alessandro Nasti, Shingo Inagaki, Tuyen Thuy Bich Ho, Akihiro Seki, Keiko Yoshida, Kosuke Satomura, Yoshio Sakai, Shuichi Kaneko, Taro Yamashita

Abstract read
In one paragraph

Article in Molecular oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. 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

9 authors.

Alessandro NastiInformation-Based Medicine Development, Graduate School of Medical Sciences, Kanazawa University, Japan.ORCID https://orcid.org/0000-0003-2550-2317
Shingo InagakiSystem Biology, Graduate School of Advanced Preventive Medical Sciences, Kanazawa University, Japan.
Tuyen Thuy Bich HoInformation-Based Medicine Development, Graduate School of Medical Sciences, Kanazawa University, Japan.
Akihiro SekiDepartment of Gastroenterology, Kanazawa University Hospital, Japan.
Keiko YoshidaSystem Biology, Graduate School of Advanced Preventive Medical Sciences, Kanazawa University, Japan.
Kosuke SatomuraSystem Biology, Graduate School of Advanced Preventive Medical Sciences, Kanazawa University, Japan.
Yoshio SakaiSystem Biology, Graduate School of Advanced Preventive Medical Sciences, Kanazawa University, Japan.
Shuichi KanekoInformation-Based Medicine Development, Graduate School of Medical Sciences, Kanazawa University, Japan.
Taro YamashitaSystem Biology, Graduate School of Advanced Preventive Medical Sciences, Kanazawa University, Japan.

Funding

Japan Society for the Promotion of Science 23K15035
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is a disease with poor prognosis due to diagnostic and therapeutic limitations. We previously identified cystatin A (CSTA) as a PDAC biomarker and have conducted the present study to investigate the antitumor effects of CSTA. PDAC murine models were established with genetically modified PAN02 tumor cell lines to evaluate the antitumor immune response. PDAC mouse survival was significantly longer with CSTA, and its antitumor effect was mediated mainly by CD4+ cells and partly by CD8+ cells. We also observed an increased infiltration of CD4+ and CD8+ cells in tumors of mice overexpressing CSTA. Phenotypically, we confirmed higher T helper type 1 (Th1) cell activity and increased frequency and activity of M1 macrophages and dendritic cells (DCs) in CSTA-overexpressing mice. Gene expression analysis highlighted pathways related to interferon gamma (IFN-γ) induction and Th1 lymphocyte activation that were induced by CSTA. Macrophages and DCs shifted toward proinflammatory antitumor phenotypes. Furthermore, activated splenocytes of PDAC model mice expressing CSTA had increased proapoptotic activity. CSTA also promoted the selective migration of CD4+ and CD11c+ immune cells in an in vitro migration assay. In conclusion, CSTA exerts antitumor effects by enhancing Th1-mediated antitumor effects through promotion of DC and M1 macrophage activity, thereby increasing immune cell chemotaxis. CSTA could be a novel therapeutic candidate for PDAC.

Indexed as

Carcinoma, Pancreatic DuctalDendritic CellsPancreatic NeoplasmsTh1 CellsAnimalsCell Line, TumorDisease Models, AnimalHumansMacrophagesMiceMice, Inbred C57BLantitumorCD4+ T cellsCSTAcystatin ADCsdendritic cellsPDACrecruitmentTh1 response

Identifiers

PMID39792573
PMCPMC12077287

What Socratic 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 Socratic graph.