Evidence map›Paper›PMID 37397541›Full record

ArticleGenes & diseases2023

Suppression of osteosarcoma progression by engineered lymphocyte-derived proteomes.

Kexin Li, Xun Sun, Hudie Li, Hailan Ma, Meng Zhou, Kazumasa Minami, Keisuke Tamari, Kazuhiko Ogawa, Pankita H Pandya, M Reza Saadatzadeh and 4 more

Abstract read
In one paragraph

Article in Genes & diseases, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

  1. Review
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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

14 authors.

Kexin LiDepartment of Pharmacology, School of Pharmacy, Harbin Medical University, Harbin, Heilongjiang 150081, China.
Xun SunDepartment of Pharmacology, School of Pharmacy, Harbin Medical University, Harbin, Heilongjiang 150081, China.
Hudie LiDepartment of Pharmacology, School of Pharmacy, Harbin Medical University, Harbin, Heilongjiang 150081, China.
Hailan MaDepartment of Pharmacology, School of Pharmacy, Harbin Medical University, Harbin, Heilongjiang 150081, China.
Meng ZhouDepartment of Pharmacology, School of Pharmacy, Harbin Medical University, Harbin, Heilongjiang 150081, China.
Kazumasa MinamiDepartment of Radiation Oncology, Osaka University Graduate School of Medicine, Suita, Osaka 565-0871, Japan.
Keisuke TamariDepartment of Radiation Oncology, Osaka University Graduate School of Medicine, Suita, Osaka 565-0871, Japan.
Kazuhiko OgawaDepartment of Radiation Oncology, Osaka University Graduate School of Medicine, Suita, Osaka 565-0871, Japan.
Pankita H PandyaSimon Comprehensive Cancer Center, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
M Reza SaadatzadehSimon Comprehensive Cancer Center, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Melissa A KacenaSimon Comprehensive Cancer Center, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Karen E PollokSimon Comprehensive Cancer Center, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Bai-Yan LiDepartment of Pharmacology, School of Pharmacy, Harbin Medical University, Harbin, Heilongjiang 150081, China.
Hiroki YokotaDepartment of Biomedical Engineering, Indiana University Purdue University Indianapolis, Indianapolis, IN 46202, USA.

Funding

Tumor Microenvironment and Metastasis ProgramP30CA082709 · NCI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI David W Clapp · 1999 to 2026
$59.3M
Project 2: Biomarkers of endothelial dysfunction in pediatric patients receiving high intensity chemotherapy/irradiationP50HD090215 · NICHD · INDIANA UNIVERSITY INDIANAPOLIS · PI PACZESNY, SOPHIE · 2019 to 2020
$1.4M
NCI NIH HHS P30 CA082709NICHD NIH HHS P50 HD090215
6 · The paper itself

Abstract

Cancer cells tend to develop resistance to chemotherapy and enhance aggressiveness. A counterintuitive approach is to tame aggressiveness by an agent that acts opposite to chemotherapeutic agents. Based on this strategy, induced tumor-suppressing cells (iTSCs) have been generated from tumor cells and mesenchymal stem cells. Here, we examined the possibility of generating iTSCs from lymphocytes by activating PKA signaling for suppressing the progression of osteosarcoma (OS). While lymphocyte-derived CM did not present anti-tumor capabilities, the activation of PKA converted them into iTSCs. Inhibiting PKA conversely generated tumor-promotive secretomes. In a mouse model, PKA-activated CM suppressed tumor-induced bone destruction. Proteomics analysis revealed that moesin (MSN) and calreticulin (Calr), which are highly expressed intracellular proteins in many cancers, were enriched in PKA-activated CM, and they acted as extracellular tumor suppressors through CD44, CD47, and CD91. The study presented a unique option for cancer treatment by generating iTSCs that secret tumor-suppressive proteins such as MSN and Calr. We envision that identifying these tumor suppressors and predicting their binding partners such as CD44, which is an FDA-approved oncogenic target to be inhibited, may contribute to developing targeted protein therapy.

Indexed as

CalreticulinLymphocytesMoesinOsteosarcomaPKAProteome

Identifiers

PMID37397541
PMCPMC10311056

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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.