Evidence map›Paper›PMID 39171141›Full record

ArticleMolecular therapy. Nucleic acids2024

Adenovirus expressing nc886, an anti-interferon and anti-apoptotic non-coding RNA, is an improved gene delivery vector.

Enkhjin Saruuldalai, Hwi-Ho Lee, Yeon-Su Lee, Eun Kyung Hong, Soyoun Ro, Yeochan Kim, TaeJin Ahn, Jong-Lyul Park, Seon-Young Kim, Seung-Phil Shin and 9 more

Abstract read
In one paragraph

Article in Molecular therapy. Nucleic acids, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. 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

19 authors.

Enkhjin SaruuldalaiDepartment of Cancer Biomedical Science, Graduate School of Cancer Science and Policy, National Cancer Center, Goyang 10408, Korea.
Hwi-Ho LeeDepartment of Cancer Biomedical Science, Graduate School of Cancer Science and Policy, National Cancer Center, Goyang 10408, Korea.
Yeon-Su LeeDivision of Rare Cancer, Research Institute, National Cancer Center, Goyang 10408, Korea.
Eun Kyung HongResearch Institute and Hospital, National Cancer Center, Goyang 10408, Korea.
Soyoun RoDivision of Immuno-Oncology, Research Institute, National Cancer Center, Goyang 10408, Korea.
Yeochan KimDepartment of Life Science, Handong Global University, Pohang 37554, Korea.
TaeJin AhnDepartment of Life Science, Handong Global University, Pohang 37554, Korea.
Jong-Lyul ParkPersonalized Genomic Medicine Research Center, KRIBB, Daejeon 34141, Korea.
Seon-Young KimPersonalized Genomic Medicine Research Center, KRIBB, Daejeon 34141, Korea.
Seung-Phil ShinDivision of Immuno-Oncology, Research Institute, National Cancer Center, Goyang 10408, Korea.
Wonkyun Ronny ImDepartment of Cancer Biomedical Science, Graduate School of Cancer Science and Policy, National Cancer Center, Goyang 10408, Korea.
Eunjung ChoDivision of Immuno-Oncology, Research Institute, National Cancer Center, Goyang 10408, Korea.
Beom K ChoiDivision of Immuno-Oncology, Research Institute, National Cancer Center, Goyang 10408, Korea.
Jiyoung Joan JangDepartment of Cancer Biomedical Science, Graduate School of Cancer Science and Policy, National Cancer Center, Goyang 10408, Korea.
Byung-Han ChoiDepartment of Cancer Biomedical Science, Graduate School of Cancer Science and Policy, National Cancer Center, Goyang 10408, Korea.
Yuh-Seog JungDivision of Immuno-Oncology, Research Institute, National Cancer Center, Goyang 10408, Korea.
In-Hoo KimDepartment of Cancer Biomedical Science, Graduate School of Cancer Science and Policy, National Cancer Center, Goyang 10408, Korea.
Sang-Jin LeeDivision of Immuno-Oncology, Research Institute, National Cancer Center, Goyang 10408, Korea.
Yong Sun LeeDepartment of Cancer Biomedical Science, Graduate School of Cancer Science and Policy, National Cancer Center, Goyang 10408, Korea.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recombinant adenovirus (rAdV) vector is the most promising vehicle to deliver an exogenous gene into target cells and is preferred for gene therapy. Exogenous gene expression from rAdV is often too inefficient to induce phenotypic changes and the amount of administered rAdV must be very high to achieve a therapeutic dose. However, it is often hampered because a high dose of rAdV is likely to induce cytotoxicity by activating immune responses. nc886, a 102-nucleotide non-coding RNA that is transcribed by RNA polymerase III, acts as an immune suppressor and a facilitator of AdV entry into the nucleus. Therefore, in this study, we have constructed an rAdV expressing nc886 (AdV:nc886) to explore whether AdV:nc886 overcomes the aforementioned drawbacks of conventional rAdV vectors. When infected into mouse cell lines and mice, AdV:nc886 expresses a sufficient amount of nc886, which suppresses the induction of interferon-stimulated genes and apoptotic pathways triggered by AdV infection. As a result, AdV:nc886 is less cytotoxic and produces more rAdV-delivered gene products, compared with the parental rAdV vector lacking nc886. In conclusion, this study demonstrates that the nc886-expressing rAdV could become a superior gene delivery vehicle with greater safety and higher efficiency for

Indexed as

adenoviruscytotoxicitygene therapyinterferonMT: Non-coding RNAsnc886

Identifiers

PMID39171141
PMCPMC11338102

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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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 Socratic graph.