Evidence map›Paper›PMID 37894284›Full record

ArticleCancers2023

Exploring the Tumor-Suppressing Potential of PSCA in Pancreatic Ductal Adenocarcinoma.

Kexin Li, Qingji Huo, Kazumasa Minami, Keisuke Tamari, Kazuhiko Ogawa, Sungsoo Na, Melissa L Fishel, Bai-Yan Li, Hiroki Yokota

Open access · goldAbstract read
In one paragraph

Article in Cancers, 2023. 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
0.5field-weighted citation impact, top 26% of its field
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, 2 citations in OpenAlex.

  1. Review
  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 at 4 institutions in 3 countries.

Kexin LiDepartment of Pharmacology, School of Pharmacy, Harbin Medical University, Harbin 150081, China.
Qingji HuoDepartment of Pharmacology, School of Pharmacy, Harbin Medical University, Harbin 150081, China.
Kazumasa MinamiDepartment of Radiation Oncology, Graduate School of Medicine, Osaka University, Suita 565-0871, Osaka, Japan.ORCID 0000-0002-3864-6478
Keisuke TamariDepartment of Radiation Oncology, Graduate School of Medicine, Osaka University, Suita 565-0871, Osaka, Japan.
Kazuhiko OgawaDepartment of Radiation Oncology, Graduate School of Medicine, Osaka University, Suita 565-0871, Osaka, Japan.
Sungsoo NaDepartment of Biomedical Engineering, Indiana University-Purdue University Indianapolis, Indianapolis, IN 46202, USA.
Melissa L FishelDepartment of Pediatrics, Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202, USA.ORCID 0000-0002-9436-6382
Bai-Yan LiDepartment of Pharmacology, School of Pharmacy, Harbin Medical University, Harbin 150081, China.ORCID 0000-0002-1853-0216
Hiroki YokotaDepartment of Biomedical Engineering, Indiana University-Purdue University Indianapolis, Indianapolis, IN 46202, USA.ORCID 0000-0002-7881-8959
The University of Osaka · JPUniversity of Indianapolis · USIndiana University Health · USHarbin Medical University · CN

Funding

Tumor Microenvironment and Metastasis ProgramP30CA082709 · NCI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI David W Clapp · 1999 to 2026
$59.3M
Novel Role of Ref-1 in Pancreatic Cancer Etiology and ProgressionR01CA167291 · NCI · INDIANA UNIVERSITY INDIANAPOLIS · PI FISHEL, MELISSA L., KELLEY, MARK R. · 2013 to 2022
$5.2M
Reprogramming PDAC Stroma by Targeting Coagulation in the Tumor MicroenvironmentU01CA274304 · NCI · UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN · PI Melissa L. Fishel, Matthew J. Flick · 2022 to 2026
$4.6M
Targeting the Plasminogen Activation System to Limit Pancreatic Cancer Progression and Associated ThrombosisU01HL143403 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI FISHEL, MELISSA L., FLICK, MATTHEW J. · 2018 to 2022
$4.2M
Investigation of novel signaling protein in 3D and in vivo PDAC models using second generation Ref-1 inhibitorsR01CA254110 · NCI · INDIANA UNIVERSITY INDIANAPOLIS · PI FISHEL, MELISSA L., HAN, BUMSOO · 2021 to 2025
$2.1M
Metabolic flux analysis and PDX models to understand therapeutic vulnerabilities following inhibition of Ref-1 redox signaling in pancreatic cancerR01CA282478 · NCI · INDIANA UNIVERSITY INDIANAPOLIS · PI Melissa L. Fishel, Mark R. Kelley · 2023 to 2026
$2.1M
A Fragment-Based Strategy for K-RAS Covalent InhibitorsR01CA264471 · NCI · UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN · PI MEROUEH, SAMY · 2021 to 2024
$1.9M
NCI NIH HHS P30 CA082709NCI NIH HHS R01 CA167291NCI NIH HHS R01CA167291NCI NIH HHS R01 CA254110NCI NIH HHS R01 CA264471NCI NIH HHS R01CA264471NCI NIH HHS R01 CA282478NCI NIH HHS U01 CA274304NHLBI NIH HHS U01 HL143403
6 · The paper itself

Abstract

Pancreatic ductal adenocarcinoma (PDAC) is an aggressive cancer with low survival rates. We explored an innovative therapeutic approach by leveraging prognostic oncogenic markers. Instead of inhibiting these marker genes, we harnessed their tumor-modifying potential in the extracellular domain. Surprisingly, many of the proteins highly expressed in PDAC, which is linked to poor survival, exhibited tumor-suppressing qualities in the extracellular environment. For instance, prostate stem cell antigens (PSCA), associated with reduced survival, acted as tumor suppressors when introduced extracellularly. We performed in vitro assays to assess the proliferation and migration and evaluated the tumor-modifying capacity of extracellular factors from peripheral blood mononuclear cells (PBMCs) in PDAC tissues. Molecular docking analysis, immunoprecipitation, Western blotting, and RNA interference were employed to study the regulatory mechanism. Extracellular PSCA recombinant protein notably curtailed the viability, motility, and transwell invasion of PDAC cells. Its anti-PDAC effects were partially mediated by Mesothelin (MSLN), another highly expressed tumor-associated antigen in PDAC. The anti-tumor effects of extracellular PSCA complemented those of chemotherapeutic agents like Irinotecan, 5-Fluorouracil, and Oxaliplatin. PSCA expression increased in a conditioned medium derived from PBMCs and T lymphocytes. This study unveils the paradoxical anti-PDAC potential of PSCA, hinting at the dual roles of oncoproteins like PSCA in PDAC suppression.

Indexed as

lymphocytesMSLNpancreatic cancerPBMCsPSCA

Identifiers

PMID37894284
PMCPMC10605218
OpenAlexW4387496711

What OpenQuestion holds

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Registered trials

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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.