Evidence map›Paper›PMID 41950246›Full record

ArticlePloS one2026

Engineering exosomes with iRGD for targeted RNAi therapy against pancreatic cancer mediated by long non-coding RNA PLBD1-AS1.

Wenbo Zhu, Xintong Zhao, Weina Hao, Xianzhu Zhou, Congjia Ma, Jiayu Chen, Yating Zhao, Xiangyu Kong, Yiqi Du, Lei Li

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2026. 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. Review
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

10 authors.

Wenbo ZhuDepartment of Gastroenterology, Changhai Hospital, Naval Medical University, Shanghai, China.
Xintong ZhaoDepartment of Gastroenterology, Changhai Hospital, Naval Medical University, Shanghai, China.
Weina HaoDepartment of Gastroenterology, Changhai Hospital, Naval Medical University, Shanghai, China.
Xianzhu ZhouDepartment of Gastroenterology, Changhai Hospital, Naval Medical University, Shanghai, China.
Congjia MaDepartment of Gastroenterology, Changhai Hospital, Naval Medical University, Shanghai, China.
Jiayu ChenDepartment of Gastroenterology, Changhai Hospital, Naval Medical University, Shanghai, China.
Yating ZhaoDepartment of Gastroenterology, Changhai Hospital, Naval Medical University, Shanghai, China.
Xiangyu KongDepartment of Gastroenterology, Changhai Hospital, Naval Medical University, Shanghai, China.
Yiqi DuDepartment of Gastroenterology, Changhai Hospital, Naval Medical University, Shanghai, China.ORCID https://orcid.org/0000-0002-4261-6888
Lei LiDigestive Endoscopy Center, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China.ORCID https://orcid.org/0009-0007-5458-766X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor-derived exosomes play critical roles in pancreatic ductal adenocarcinoma (PDAC) progression by mediating intercellular communication within the tumor microenvironment. This study identifies the long non-coding RNA PLBD1-AS1 as a functional oncogenic lncRNA enriched in PDAC exosomes. We demonstrate that PLBD1-AS1 promotes tumor cell proliferation, migration, and invasion by interacting with the glycolytic enzyme ALDOA and enhancing glycolytic flux. Furthermore, tumor exosomes deliver PLBD1-AS1 to pancreatic stellate cells (PSC), augmenting their glycolysis and facilitating their activation into cancer-associated fibroblasts, thereby shaping a pro-tumorigenic microenvironment. To target it, we developed an engineered exosome system modified with the tumor-penetrating peptide iRGD for specific delivery of siPLBD1-AS1 to both tumor and stromal cells. The resulting iRGD-exo-siPLBD1-AS1 construct demonstrated enhanced cellular uptake and effectively suppressed PLBD1-AS1 expression, inhibited glycolysis, impaired PSC activation, and significantly attenuated tumor growth. Our findings reveal a novel mechanism of exosome-mediated metabolic crosstalk in PDAC and establish a promising RNAi-based therapeutic strategy targeting this lethal malignancy.

Indexed as

Carcinoma, Pancreatic DuctalExosomesOligopeptidesPancreatic NeoplasmsRNA InterferenceRNAi TherapeuticsRNA, Long NoncodingAnimalsCell Line, TumorCell MovementCell ProliferationGlycolysisHumansMiceMice, NudePancreatic Stellate CellsOligopeptidesRNA, Long Noncoding

Identifiers

PMID41950246
PMCPMC13061246

What OpenQuestion holds

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LicenceCC BY
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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.