Evidence map›Paper›PMID 30088967›Full record

ArticleNucleic acid therapeutics2018

MicroRNAs Enable mRNA Therapeutics to Selectively Program Cancer Cells to Self-Destruct.

Ruchi Jain, Josh P Frederick, Eric Y Huang, Kristine E Burke, David M Mauger, Elizaveta A Andrianova, Sam J Farlow, Summar Siddiqui, Jeffrey Pimentel, Kahlin Cheung-Ong and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Nucleic acid therapeutics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

91 citing papers in PubMed, 154 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. "More" Artificial mRNAs: Beyond the Art of Nature.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  13. Article
  14. Article
  15. Article
  16. mRNA vaccines for gastrointestinal cancers: a paradigm shift in treatment.Naunyn-Schmiedeberg's archives of pharmacology · 2026
    Review
  17. Article
  18. Review
  19. Article
  20. Article

31 more citing papers are in PubMed but not listed here.

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 at 1 institution in 1 country.

Ruchi Jain1 Department of Molecular Biology, Moderna Therapeutics , Cambridge, Massachusetts.
Josh P Frederick2 Department of Oncology, Moderna Therapeutics , Cambridge, Massachusetts.
Eric Y Huang3 New Venture Labs , Moderna Therapeutics, Cambridge, Massachusetts.
Kristine E Burke4 Non-Clinical Sciences , Moderna Therapeutics, Cambridge, Massachusetts.
David M Mauger5 Computational Sciences , Moderna Therapeutics, Cambridge, Massachusetts.
Elizaveta A Andrianova1 Department of Molecular Biology, Moderna Therapeutics , Cambridge, Massachusetts.
Sam J Farlow2 Department of Oncology, Moderna Therapeutics , Cambridge, Massachusetts.
Summar Siddiqui6 Rare Diseases , Moderna Therapeutics, Cambridge, Massachusetts.
Jeffrey Pimentel6 Rare Diseases , Moderna Therapeutics, Cambridge, Massachusetts.
Kahlin Cheung-Ong2 Department of Oncology, Moderna Therapeutics , Cambridge, Massachusetts.
Kristine M McKinney3 New Venture Labs , Moderna Therapeutics, Cambridge, Massachusetts.
Caroline Köhrer1 Department of Molecular Biology, Moderna Therapeutics , Cambridge, Massachusetts.
Melissa J Moore1 Department of Molecular Biology, Moderna Therapeutics , Cambridge, Massachusetts.
Tirtha Chakraborty1 Department of Molecular Biology, Moderna Therapeutics , Cambridge, Massachusetts.
Moderna Therapeutics (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The advent of therapeutic mRNAs significantly increases the possibilities of protein-based biologics beyond those that can be synthesized by recombinant technologies (eg, monoclonal antibodies, extracellular enzymes, and cytokines). In addition to their application in the areas of vaccine development, immune-oncology, and protein replacement therapies, one exciting possibility is to use therapeutic mRNAs to program undesired, diseased cells to synthesize a toxic intracellular protein, causing cells to self-destruct. For this approach to work, however, methods are needed to limit toxic protein expression to the intended cell type. Here, we show that inclusion of microRNA target sites in therapeutic mRNAs encoding apoptotic proteins, Caspase or PUMA, can prevent their expression in healthy hepatocytes while triggering apoptosis in hepatocellular carcinoma cells.

Indexed as

AnimalsApoptosisApoptosis Regulatory ProteinsCarcinoma, HepatocellularCaspasesGene Expression Regulation, NeoplasticHeLa CellsHepatocytesHumansLiver NeoplasmsMiceMicroRNAsPrimary Cell CultureProto-Oncogene ProteinsRAW 264.7 CellsRNA, MessengerApoptosis Regulatory ProteinsBBC3 protein, humanCaspasesMicroRNAsProto-Oncogene ProteinsRNA, MessengermiRNAmRNARNA modificationssuicide therapytherapeutic

Identifiers

PMID30088967
PMCPMC6157376
OpenAlexW2885809926

What OpenQuestion 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 OpenQuestion graph.