Evidence map›Paper›PMID 30759826›Full record

ArticleMolecules (Basel, Switzerland)2019

Cucurbitacin B Induces the Lysosomal Degradation of EGFR and Suppresses the CIP2A/PP2A/Akt Signaling Axis in Gefitinib-Resistant Non-Small Cell Lung Cancer.

Pengfei Liu, Yuchen Xiang, Xuewen Liu, Te Zhang, Rui Yang, Sen Chen, Li Xu, Qingqing Yu, Huzi Zhao, Liang Zhang and 2 more

Open access · goldAbstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
5.4field-weighted citation impact, top 4% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
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  6. Article
  7. Recent Advances in the Application of Cucurbitacin B as an Anticancer Agent.International journal of molecular sciences · 2025
    Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. A Scoping Review on Cucumis melo and Its Anti-Cancer Properties.The Malaysian journal of medical sciences : MJMS · 2024
    Article
  13. Phytochemicals Target Multiple Metabolic Pathways in Cancer.Antioxidants (Basel, Switzerland) · 2023
    Review
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  15. Review
  16. Article
  17. Review
  18. Article
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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

12 authors at 1 institution in 1 country.

Pengfei LiuLaboratory of Molecular Target Therapy of Cancer, Institute of Basic Medical Sciences, Hubei University of Medicine, Shiyan 442000, China. LiuPF_001@163.com.
Yuchen XiangLaboratory of Molecular Target Therapy of Cancer, Institute of Basic Medical Sciences, Hubei University of Medicine, Shiyan 442000, China. xiangyc4026@163.com.
Xuewen LiuLaboratory of Molecular Target Therapy of Cancer, Institute of Basic Medical Sciences, Hubei University of Medicine, Shiyan 442000, China. liuxw1110@163.com.
Te ZhangLaboratory of Molecular Target Therapy of Cancer, Biomedical Research Institute, Hubei University of Medicine, Shiyan 442000, China. zhangte519@163.com.
Rui YangLaboratory of Molecular Target Therapy of Cancer, Institute of Basic Medical Sciences, Hubei University of Medicine, Shiyan 442000, China. yangr0512@163.com.
Sen ChenLaboratory of Molecular Target Therapy of Cancer, Institute of Basic Medical Sciences, Hubei University of Medicine, Shiyan 442000, China. sener_chen@163.com.
Li XuLaboratory of Molecular Target Therapy of Cancer, Biomedical Research Institute, Hubei University of Medicine, Shiyan 442000, China. xuli103028@sina.com.
Qingqing YuLaboratory of Molecular Target Therapy of Cancer, Biomedical Research Institute, Hubei University of Medicine, Shiyan 442000, China. 18064081841@163.com.
Huzi ZhaoLaboratory of Molecular Target Therapy of Cancer, Institute of Basic Medical Sciences, Hubei University of Medicine, Shiyan 442000, China. zhaohz07@163.com.
Liang ZhangLaboratory of Molecular Target Therapy of Cancer, Institute of Basic Medical Sciences, Hubei University of Medicine, Shiyan 442000, China. zl_19820321@163.com.
Ying LiuLaboratory of Molecular Target Therapy of Cancer, Institute of Basic Medical Sciences, Hubei University of Medicine, Shiyan 442000, China. ying_liu1002@163.com.
Yuan SiLaboratory of Molecular Target Therapy of Cancer, Institute of Basic Medical Sciences, Hubei University of Medicine, Shiyan 442000, China. siyuan138@126.com.
Hubei University of Medicine · CN

Funding

National Natural Science Foundation of China 81802387the Faculty Development grants from Hubei University of Medicine 2018QDJZR03, 2017QDJZR12, 2018QDJZR27the National Training Program of Innovation and Entrepreneurship for Undergraduates 201810929012 and 201810929056the Scientific and Technological Project of Shiyan City of Hubei Province 17Y01 and 18Y13
6 · The paper itself

Abstract

Non-small cell lung cancer (NSCLC) patients carrying an epidermal growth factor receptor (EGFR) mutation are initially sensitive to EGFR-tyrosine kinase inhibitors (TKIs) treatment, but soon develop an acquired resistance. The treatment effect of EGFR-TKIs-resistant NSCLC patients still faces challenges. Cucurbitacin B (CuB), a triterpene hydrocarbon compound isolated from plants of various families and genera, elicits anticancer effects in a variety of cancer types. However, whether CuB is a viable treatment option for gefitinib-resistant (GR) NSCLC remains unclear. Here, we investigated the anticancer effects and underlying mechanisms of CuB. We report that CuB inhibited the growth and invasion of GR NSCLC cells and induced apoptosis. The inhibitory effect of CuB occurred through its promotion of the lysosomal degradation of EGFR and the downregulation of the cancerous inhibitor of protein phosphatase 2A/protein phosphatase 2A/Akt (CIP2A/PP2A/Akt) signaling axis. CuB and cisplatin synergistically inhibited tumor growth. A xenograft tumor model indicated that CuB inhibited tumor growth in vivo. Immunohistochemistry results further demonstrated that CuB decreased EGFR and CIP2A levels in vivo. These findings suggested that CuB could suppress the growth and invasion of GR NSCLC cells by inducing the lysosomal degradation of EGFR and by downregulating the CIP2A/PP2A/Akt signaling axis. Thus, CuB may be a new drug candidate for the treatment of GR NSCLC.

Indexed as

A549 CellsAnimalsAntineoplastic AgentsApoptosisAutoantigensCarcinoma, Non-Small-Cell LungCell Line, TumorDown-RegulationDrug Resistance, NeoplasmErbB ReceptorsFemaleGefitinibGene Expression Regulation, NeoplasticHumansIntracellular Signaling Peptides and ProteinsLung NeoplasmsAntineoplastic AgentsAutoantigensCIP2A protein, humancucurbitacin BEGFR protein, humanErbB ReceptorsGefitinibIntracellular Signaling Peptides and ProteinsMembrane ProteinsProtein Kinase InhibitorsProtein Phosphatase 2Proto-Oncogene Proteins c-aktTriterpenesCIP2ACucurbitacin BEGFRgefitinib-resistant NSCLClysosomal degradation

Identifiers

PMID30759826
PMCPMC6384961
OpenAlexW2913187772

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.