Evidence map›Paper›PMID 36428672›Full record

ArticleCancers2022

N6-Methyladenosine Modification of CIRCKRT17 Initiated by METTL3 Promotes Osimertinib Resistance of Lung Adenocarcinoma by EIF4A3 to Enhance YAP1 Stability.

Ying Ji, Qing Zhao, Wei Feng, Yue Peng, Bin Hu, Qirui Chen

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancers, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

20 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Epitranscriptomic RNA mAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. New insights into the regulation of METTL3 and its role in tumors.Cell communication and signaling : CCS · 2023
    Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. 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

6 authors at 3 institutions in 1 country.

Ying JiDepartment of Thoracic Surgery, Beijing Institute of Respiratory Medicine and Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, China.
Qing ZhaoDepartment of Thoracic Surgery, Beijing Institute of Respiratory Medicine and Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, China.
Wei FengDepartment of Cardiothoracic Surgery, The Third Xiangya Hospital of Central South University, Changsha 410013, China.
Yue PengDepartment of Thoracic Surgery, Beijing Institute of Respiratory Medicine and Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, China.
Bin HuDepartment of Thoracic Surgery, Beijing Institute of Respiratory Medicine and Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, China.
Qirui ChenDepartment of Thoracic Surgery, Beijing Institute of Respiratory Medicine and Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, China.
Beijing Chao-Yang Hospital · CNCapital Medical University · CNThird Xiangya Hospital · CN

Funding

Beijing Chao-Yang Hospital Golden Seeds Foundation No. CYJZ202130
6 · The paper itself

Abstract

backgroundCircular RNAs (circRNAs) play a key role in regulating the drug resistance of numerous human tumors. However, whether circKRT17 involves in the osimertinib resistance of lung adenocarcinoma (LUAD) remains undetermined.

methodsRelative mRNA/circRNA and protein levels were detected by qRT-PCR and western blotting. Localization of circKRT17 and YAP1 was determined by FISH and immunofluorescence staining. Cell growth and apoptosis were evaluated using colony formation, EdU assays, and flow cytometry. The N6-methyladenosine (m6A) modification was analyzed by MeRIP. The interplay between EIF4A3 and circKRT17 or YAP1 was verified by RNA pull-down or/and RIP assays. Subcutaneous tumor growth was monitored in nude mice, and Ki-67 and TUNEL staining were carried out to evaluate cell proliferation and apoptosis, respectively.

resultsCircKRT17 and METTL3 were elevated in osimertinib-insensitive LUAD tissues and cells. Knockdown of circKRT 17 and METTL3 increased the sensitivity of LUAD cells to osimertinib. Knockdown of METTL3 decreased the expression of circKRT17 by inhibiting m6A modification. CircKRT17 promoted the stability and nuclear transportation of YAP1 by recruiting EIF4A3 in LUAD cells. Overexpression of YAP1 abolished the impacts of circKRT17 knockdown on the osimertinib sensitivity of LUAD cells. CircKRT17 knockdown increased the repressive effects of osimertinib on tumor growth in vivo by inhibiting YAP1 signaling.

conclusionMETTL3 initiated the m6A modification of circKRT17, thus promoting osimertinib resistance of LUAD by enhancing YAP1 stability through EIF4A4 recruitment.

Indexed as

circKRT17lung adenocarcinomam6A modificationosimertinib resistanceYAP1 signaling

Identifiers

PMID36428672
PMCPMC9688051
OpenAlexW4309032769

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.