Evidence map›Paper›PMID 29050671›Full record

ArticleThe Kaohsiung journal of medical sciences2017

Gambogic acid improves non-small cell lung cancer progression by inhibition of mTOR signaling pathway.

Teng Zhao, Hong-Jian Wang, Wen-Wen Zhao, Yi-Ling Sun, Li-Kuan Hu

Open access · goldAbstract read
In one paragraph

Article in The Kaohsiung journal of medical sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
4.6field-weighted citation impact, top 6% 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

12 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. ACS applied bio materials · 2022
    Article
  5. Review
  6. Review
  7. Article
  8. Gambogic acid: A shining natural compound to nanomedicine for cancer therapeutics.Biochimica et biophysica acta. Reviews on cancer · 2020
    Review
  9. Gambogic Acid as a Candidate for Cancer Therapy: A Review.International journal of nanomedicine · 2020
    Review
  10. Article
  11. Article
  12. Telomerase Inhibitors from Natural Products and Their Anticancer Potential.International journal of molecular sciences · 2017
    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 3 institutions in 1 country.

Teng ZhaoDepartment of Oncology, Qilu Hospital of Shandong University, Ji'nan City, Shandong Province, PR China.
Hong-Jian WangThe Second Department of Oncology, Tengzhou Central People's Hospital, Tengzhou City, Shandong Province, PR China.
Wen-Wen ZhaoShandong Maternal and Child Health Care Hospital, Ji'nan City, Shandong Province, PR China.
Yi-Ling SunThe Second Department of Oncology, Tengzhou Central People's Hospital, Tengzhou City, Shandong Province, PR China.
Li-Kuan HuDepartment of Oncology, Qilu Hospital of Shandong University, Ji'nan City, Shandong Province, PR China. Electronic address: hulikuan17305@163.com.
Qilu Hospital of Shandong University · CNTengzhou Central People's Hospital · CNShandong Maternal and Child Health Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gambogic acid (GA) has been shown to inhibit cancer cell proliferation, induce apoptosis, and enhance reactive oxygen species accumulation. However, whether GA could improve multidrug resistance through modulating autophagy has never been explored. We demonstrated that the combination of GA and cisplatin (CDDP) resulted in a stronger growth inhibition effect on A549 and NCI-H460 cells using the MTT assay. Furthermore, treatment with GA significantly increased autophagy in these cells. More importantly, GA-induced cell death could be largely abolished by 3-methyladenine (3-MA) or chloroquine (CQ) treatment, suggesting that GA-induced cell death was dependent on autophagy. Western blot analysis showed that GA treatment suppressed the activation of Akt, mTOR, and S6. In addition, using a GA and rapamycin combination induced more cell death compared to either GA or rapamycin alone. In summary, GA may have utility as an adjunct therapy for non-small cell lung cancer (NSCLC) patients through autophagy-dependent cell death, even when cancer cells have developed resistance to apoptosis.

Indexed as

Gene Expression Regulation, NeoplasticA549 CellsAdenineAntineoplastic Agents, PhytogenicAutophagyCell Line, TumorCell ProliferationChloroquineCisplatinDrug CombinationsDrug SynergismGarciniaHumansMicrotubule-Associated ProteinsPlant ExtractsProto-Oncogene Proteins c-akt3-methyladenineAdenineAntineoplastic Agents, PhytogenicChloroquineCisplatinDrug Combinationsgambogic acidMAP1LC3A protein, humanMicrotubule-Associated ProteinsMTOR protein, humanPlant ExtractsProto-Oncogene Proteins c-aktRibosomal Protein S6SirolimusTOR Serine-Threonine KinasesXanthonesAutophagyCell deathGambogic acidMultidrug resistance

Identifiers

PMID29050671
PMCPMC11915912
OpenAlexW2737989983

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.