Evidence map›Paper›PMID 33202255›Full record

ArticlePharmacological research2021

A CRISPR-Cas9 repressor for epigenetic silencing of KRAS.

Jingwen Liu, Meiyan Sun, Kwang Bog Cho, Xiang Gao, Bin Guo

Open access · greenAbstract read
In one paragraph

Article in Pharmacological research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

17 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. CRISPR Interference to Inhibit Oncogenes for Cancer Therapy.International journal of molecular sciences · 2026
    Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. CRISPRingCancers · 2024
    Review
  8. Article
  9. Review
  10. Advances in CRISPR therapeutics.Nature reviews. Nephrology · 2023
    Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. CRISPR and KRAS: a match yet to be made.Journal of biomedical science · 2021
    Review
  17. 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

5 authors at 2 institutions in 2 countries.

Jingwen LiuDepartment of Pharmacological and Pharmaceutical Sciences, University of Houston, Houston, TX, 77204, United States.
Meiyan SunDepartment of Pharmacological and Pharmaceutical Sciences, University of Houston, Houston, TX, 77204, United States; College of Laboratory Medicine, Jilin Medical University, Jilin Province, 132013, China. Electronic address: sunmy990@163.com.
Kwang Bog ChoDepartment of Pharmacological and Pharmaceutical Sciences, University of Houston, Houston, TX, 77204, United States.
Xiang GaoDepartment of Pharmacological and Pharmaceutical Sciences, University of Houston, Houston, TX, 77204, United States.
Bin GuoDepartment of Pharmacological and Pharmaceutical Sciences, University of Houston, Houston, TX, 77204, United States. Electronic address: bguo3@uh.edu.
University of Houston · USJilin Medical University · CN

Funding

RNA Therapeutics for Targeted Treatment of Colon CancerR01CA186100 · NCI · UNIVERSITY OF HOUSTON · PI GUO, BIN · 2015 to 2018
$1.4M
NCI NIH HHS R01 CA186100
6 · The paper itself

Abstract

KRAS is one of the most frequently mutated oncogenes in cancers. Currently no direct and effective anti-KRAS therapies are available. Using the powerful CRISPR-Cas9 technology to target the mutant KRAS promoter, we designed an epigenetic repressor to silence KRAS through epigenome editing. Catalytically dead Cas9 (dCas9) functioned as a DNA binding device, which was fused with a transcriptional repressor histone deacetylase 1 (HDAC1). We designed a panel of three CRISPR RNAs (crRNAs) covering 1500-bp range of the KRAS promoter and identified that crRNA1 and crRNA2 efficiently silenced KRAS. The suppression of K-Ras resulted in a significant inhibition of cell growth, suppression of colony formation in soft agar and induction of cell death in cancer cells with KRAS mutations. In addition, the chromatin immunoprecipitation (ChIP) assay demonstrated dCas9-HDAC1 modified histone acetylation on the KRAS promoter. Furthermore, transfection of dCas9-HDAC1 protein and gRNA ribonucleoprotein complex also inhibited K-Ras and suppressed cell proliferation. In summary, we have developed a new strategy that combines CRISPR-Cas9 technology with HDAC1 epigenetic silencing to target cancers driven by KRAS mutations.

Indexed as

CRISPR-Cas SystemsAcetylationApoptosisCell Line, TumorCell ProliferationGene EditingHistone Deacetylase 1HistonesHumansNeoplasmsProto-Oncogene Proteins p21(ras)HDAC1 protein, humanHistone Deacetylase 1HistonesKRAS protein, humanProto-Oncogene Proteins p21(ras)CRISPREpigeneticsHDAC1KRAS mutationsRibonucleoprotein

Identifiers

PMID33202255
PMCPMC8422974
OpenAlexW3099076236

What OpenQuestion holds

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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.