Evidence map›Paper›PMID 30992674›Full record

ArticleOncoTargets and therapy2019

Luteolin suppresses tumor proliferation through inducing apoptosis and autophagy via MAPK activation in glioma.

Yijie You, Rong Wang, Naiyuan Shao, Feng Zhi, Yilin Yang

Open access · goldAbstract read
In one paragraph

Article in OncoTargets and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.6field-weighted citation impact, top 10% 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, 57 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Application of Luteolin in Neoplasms and Nonneoplastic Diseases.International journal of molecular sciences · 2023
    Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Article
  17. Luteolin Induced Hippocampal Neuronal Pyroptosis Inhibition by Regulation of miR-124-3p/TNF-Evidence-based complementary and alternative medicine : eCAM · 2022
    Article
  18. Article
  19. Review
  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

5 authors at 1 institution in 1 country.

Yijie YouDepartment of Neurosurgery, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu, China, danielzhif@suda.edu.cn, yilinyang.czfph@gmail.com.
Rong WangModern Medical Research Center, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu, China, danielzhif@suda.edu.cn, yilinyang.czfph@gmail.com.
Naiyuan ShaoDepartment of Neurosurgery, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu, China, danielzhif@suda.edu.cn, yilinyang.czfph@gmail.com.
Feng ZhiDepartment of Neurosurgery, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu, China, danielzhif@suda.edu.cn, yilinyang.czfph@gmail.com.
Yilin YangDepartment of Neurosurgery, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu, China, danielzhif@suda.edu.cn, yilinyang.czfph@gmail.com.
Soochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeGlioma is a malignant tumor that originates in the brain and spine and is difficult to be completely removed. Though glioma patients receive active treatment, the survival rate is still poor. Therefore, it is urgent to discover a new medicine to treat glioma patients in order to improve the survival rate. In this study, we explored the anticancer effect and the potential mechanism of luteolin on glioma in vitro. MATERIALS AND

methodsCell viability was determined by Cell Counting Kit-8 (CCK-8) assay. Fluorescent microscopy and flow cytometry analysis were used to determine the cellular apoptosis. Western blot analysis was performed to explore the changes in protein expression. Quantitative reverse transcription-PCR (qRT-PCR) analysis was utilized to evaluate the expression level of the tumor suppressor miR-124-3p.

resultsCCK-8 assays indicated that luteolin significantly inhibited glioma cell proliferation in a time- and dose-dependent manner. Fluorescent microscopy and flow cytometry analysis confirmed that luteolin induced glioma cell apoptosis. Western blot analysis showed that luteolin induced cellular apoptosis in glioma cells via MAPK activation (JNK, ERK, and p38). Luteolin stimulated the death receptor (FADD) to regulate the apoptosis proteins (Caspase-8, Caspase-3, and PARP). Luteolin increased the expression levels of LC3B II/I and downregulated the level of p62 that promotes cell autophagy. Finally, qRT-PCR confirmed that luteolin upregulated the expression levels of miR-124-3p.

conclusionThese findings illustrate that luteolin may be a potential drug for glioma treatment.

Indexed as

apoptosisautophagygliomaluteolinmiR-124-3p

Identifiers

PMID30992674
PMCPMC6445239
OpenAlexW2923047376

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.