Evidence map›Paper›PMID 35093302›Full record

ReviewTrends in cancer2022

Interplay between K-RAS and miRNAs.

Bing Shui, Gaspare La Rocca, Andrea Ventura, Kevin M Haigis

Open access · greenAbstract readReview
In one paragraph

Review in Trends in cancer, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

18 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Identification of Oncogene-Induced Senescence-Associated MicroRNAs.Methods in molecular biology (Clifton, N.J.) · 2025
    Article
  11. Review
  12. Article
  13. Article
  14. miRNAs in pancreatic cancer progression and metastasis.Clinical & experimental metastasis · 2024
    Review
  15. Review
  16. Review
  17. Article
  18. 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

4 authors at 2 institutions in 1 country.

Bing ShuiDivision of Medical Sciences, Harvard Medical School, Boston, MA, USA; Department of Cancer Biology, Dana-Faber Cancer Institute, Boston, MA, USA; Department of Medicine, Brigham & Women's Hospital, Boston, MA, USA; Department of Medicine, Harvard Medical School, Boston, MA, USA.
Gaspare La RoccaCancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Andrea VenturaCancer Biology and Genetics Program, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Kevin M HaigisDepartment of Cancer Biology, Dana-Faber Cancer Institute, Boston, MA, USA; Department of Medicine, Brigham & Women's Hospital, Boston, MA, USA; Department of Medicine, Harvard Medical School, Boston, MA, USA. Electronic address: Kevin_Haigis@dfci.harvard.edu.
Dana-Farber Cancer Institute · USMemorial Sloan Kettering Cancer Center · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Hongbiao Carl Lekaye · 1985 to 2026
$347.4M
Investigating the functions of the miR-17~92 family of oncogenic microRNA clustersR01CA149707 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI VENTURA, ANDREA · 2010 to 2021
$3.8M
Tissue-specific genetic interactions in cancerR01CA232372 · NCI · DANA-FARBER CANCER INST · PI HAIGIS, KEVIN · 2018 to 2022
$2.9M
Investigating microRNA Function in Homeostasis, Regeneration and CancerR01CA245507 · NCI · SLOAN-KETTERING INST CAN RESEARCH · PI VENTURA, ANDREA · 2020 to 2024
$2.6M
Basic and Translational studies of Ras-mutant colorectal cancerR01CA178017 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI HAIGIS, KEVIN · 2014 to 2018
$1.8M
Cancer Research UKNCI NIH HHS P30 CA008748NCI NIH HHS R01 CA149707NCI NIH HHS R01 CA178017NCI NIH HHS R01 CA232372NCI NIH HHS R01 CA245507
6 · The paper itself

Abstract

K-RAS is frequently mutated in cancers, and its overactivation can lead to oncogene-induced senescence (OIS), a barrier to cellular transformation. Feedback onto K-RAS limits its signaling to avoid senescence while achieving the appropriate level of activation that promotes proliferation and survival. Such regulation could be mediated by miRNAs, as aberrant RAS signaling and miRNA activity coexist in several cancers, with miRNAs acting both up- and downstream of K-RAS. Several miRNAs both regulate and are regulated by K-RAS, suggesting a noncoding RNA-based feedback mechanism. Functional interactions between K-RAS and the miRNA machinery have also begun to unfold. This review comprehensively surveys the state of knowledge connecting K-RAS to miRNA function and proposes a model for the regulation of K-RAS signaling by noncoding RNAs.

Indexed as

MicroRNAsNeoplasmsCell Transformation, NeoplasticGene Expression Regulation, NeoplasticHumansSignal TransductionMicroRNAscancerfeedback regulationK-RASmiRNA

Identifiers

PMID35093302
PMCPMC9035052
OpenAlexW4210411631

What OpenQuestion holds

Textmetadata
LicenceTDM
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.