Evidence map›Paper›PMID 32576183›Full record

ArticleBMC complementary medicine and therapies2020

Ginkgolide B inhibits lung cancer cells promotion via beclin-1-dependent autophagy.

Xuan Wang, Qi-Hui Shao, Hao Zhou, Jun-Lu Wu, Wen-Qiang Quan, Ping Ji, Yi-Wen Yao, Dong Li, Zu-Jun Sun

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in BMC complementary medicine and therapies, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

13 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Antioxidants (Basel, Switzerland) · 2022
    Review
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  7. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Xuan Wang *Department of Pharmacy, Putuo People's Hospital, Shanghai, 200060, China. wxandld186@163.com.
Qi-Hui Shao *Department of Traditional Chinese Medicine, Shanghai Tongji Hospital, Tongji University School of Medicine, Shanghai, 200065, China.
Hao ZhouDepartment of Pharmacy, Putuo People's Hospital, Shanghai, 200060, China.
Jun-Lu WuDepartment of Clinical Laboratory, Shanghai Tongji Hospital, Tongji University School of Medicine, Shanghai, 200065, China.
Wen-Qiang QuanDepartment of Clinical Laboratory, Shanghai Tongji Hospital, Tongji University School of Medicine, Shanghai, 200065, China.
Ping JiDepartment of Clinical Laboratory, Shanghai Tongji Hospital, Tongji University School of Medicine, Shanghai, 200065, China.
Yi-Wen YaoDepartment of Clinical Laboratory, Shanghai Tongji Hospital, Tongji University School of Medicine, Shanghai, 200065, China.
Dong LiDepartment of Clinical Laboratory, Shanghai Tongji Hospital, Tongji University School of Medicine, Shanghai, 200065, China.
Zu-Jun SunDepartment of Clinical Laboratory, Shanghai Tongji Hospital, Tongji University School of Medicine, Shanghai, 200065, China. sunzujun@tongji.edu.cn.ORCID http://orcid.org/0000-0002-4094-9961
Tongji University · CNCentral Hospital of Putuo District · CN

Funding

National Natural Science Foundation of China 81974314
6 · The paper itself

Abstract

backgroundGinkgolide B (GKB) is a major active component of the extracts of Ginkgo biloba leaves, and it has been used as an anti-cancer agent. However, it is unknown whether GKB has the therapeutic effects on lung cancer. Here, we studied the effects of GKB on lung cancer cells.

methodsThe effects of GKB on lung cancer cell proliferation and invasion were analyzed by cell counting kit (CCK-8) and cell invasion assays, respectively. Apoptosis was detected by flow cytometry. Western blot analysis was used to confirm the expression of autophagy-associated proteins in GKB-treated cells. Immunofluorescence analysis was used to analyze the level of light chain 3B (LC3B).

resultsTreatment with GKB time-dependently inhibited the proliferation and decreased the invasive capacity of A549 and H1975 cells. GKB induced apoptosis of these cells, but there was no significant effect on apoptosis compared to the control treatment. GKB-induced inhibition of cell proliferation and GKB-induced cell death were due to autophagy rather than apoptosis. GKB-induced autophagy of lung cancer cells was dependent on beclin-1, and autophagy-induced inhibition of the NLRP3 inflammasome contributed to the anti-tumor effect of GKB.

conclusionsGKB-mediated autophagy of lung cancer cells is beclin-1-dependent and results in inhibition of the NLRP3 inflammasome. Therefore, GKB might be a potential therapeutic candidate for the treatment of lung cancer.

Indexed as

A549 CellsAntineoplastic Agents, PhytogenicApoptosisAutophagyBeclin-1Cell ProliferationGinkgolidesHumansLactonesLung NeoplasmsMolecular StructurePlant LeavesAntineoplastic Agents, PhytogenicBeclin-1BECN1 protein, humanginkgolide BGinkgolidesLactonesAutophagyBeclin-1Ginkgolide BLight chain 3BNLRP3

Identifiers

PMID32576183
PMCPMC7310550
OpenAlexW3036037320

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.