Evidence map›Paper›PMID 33247550›Full record

ArticleJournal of cellular and molecular medicine2021

Licochalcone A inhibits EGFR signalling and translationally suppresses survivin expression in human cancer cells.

Feng Gao, Ming Li, Xinfang Yu, Wenbin Liu, Li Zhou, Wei Li

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 17% 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, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Panduratin A fromInternational journal of molecular sciences · 2025
    Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Anticancer Potential of Natural Chalcones: In Vitro and In Vivo Evidence.International journal of molecular sciences · 2023
    Review
  12. Article
  13. Article
  14. Anticancer Activity of Natural and Synthetic Chalcones.International journal of molecular sciences · 2021
    Review
  15. Review
  16. Review
  17. 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 2 institutions in 2 countries.

Feng GaoDepartment of Ultrasonography, The Third Xiangya Hospital of Central South University, Changsha, China.
Ming LiCell Transplantation and Gene Therapy Institute, The 3rd Xiangya Hospital of Central South University, Changsha, China.
Xinfang YuCell Transplantation and Gene Therapy Institute, The 3rd Xiangya Hospital of Central South University, Changsha, China.
Wenbin LiuDepartment of Pathology, Hunan Cancer Hospital, Changsha, China.
Li ZhouDepartment of Pathology, Xiangya Hospital of Central South University, Changsha, China.
Wei LiCell Transplantation and Gene Therapy Institute, The 3rd Xiangya Hospital of Central South University, Changsha, China.ORCID 0000-0002-7267-6494
Central South University · CNHunan Cancer Hospital · CN

Funding

National Natural Science Foundation of China 81401548National Natural Science Foundation of China 81972837Natural Science Foundation of Hunan Province 2018JJ2604Natural Science Foundation of Hunan Province 2018JJ3787
6 · The paper itself

Abstract

Dysfunction of epidermal growth factor receptor (EGFR) signalling plays a critical role in the oncogenesis of non-small-cell lung cancer (NSCLC). Here, we reported the natural product, licochalcone A, exhibited a profound anti-tumour efficacy through directly targeting EGFR signalling. Licochalcone A inhibited in vitro cell growth, colony formation and in vivo tumour growth of either wild-type (WT) or activating mutation EGFR-expressed NSCLC cells. Licochalcone A bound with L858R single-site mutation, exon 19 deletion, L858R/T790M mutation and WT EGFR ex vivo, and impaired EGFR kinase activity both in vitro and in NSCLC cells. The in silico docking study further indicated that licochalcone A interacted with both WT and mutant EGFRs. Moreover, licochalcone A induced apoptosis and decreased survivin protein robustly in NSCLC cells. Mechanistically, we found that treatment with licochalcone A translationally suppressed survivin through inhibiting EGFR downstream kinases ERK1/2 and Akt. Depletion of the translation initiation complex by eIF4E knockdown effectively inhibited survivin expression. In contrast, knockdown of 4E-BP1 showed the opposite effect and dramatically enhanced survivin protein level. Overall, our data indicate that targeting survivin might be an alternative strategy to sensitize EGFR-targeted therapy.

Indexed as

AcrylamidesAniline CompoundsAntineoplastic AgentsBlotting, WesternCarcinoma, Non-Small-Cell LungChalconesErbB ReceptorsExonsFlow CytometryHumansImmunohistochemistryIndolesMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3MutationProto-Oncogene Proteins c-aktAcrylamidesAniline CompoundsAntineoplastic AgentsChalconesEGFR protein, humanErbB ReceptorsIndoleslicochalcone AMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3osimertinibProto-Oncogene Proteins c-aktPyrimidinesSurvivinepidermal growth factor receptorlicochalcone Anon-small-cell lung cancersurvivin

Identifiers

PMID33247550
PMCPMC7812290
OpenAlexW3110263622

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.