Evidence map›Paper›PMID 30797236›Full record

ArticleBiological research2019

Vitexin induces apoptosis through mitochondrial pathway and PI3K/Akt/mTOR signaling in human non-small cell lung cancer A549 cells.

Xiaoli Liu, Qingfeng Jiang, Huaimin Liu, Suxia Luo

Open access · goldAbstract read
In one paragraph

Article in Biological research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 1 pooled it
5.1field-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

58 citing papers in PubMed, 1 synthesis or guideline pooled it, 129 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. The Therapeutic Potential ofMolecules (Basel, Switzerland) · 2025
    Article
  7. Review
  8. Review
  9. Article
  10. Molecular Mechanisms of Vitexin: An Update on Its Anti-Cancer Functions.International journal of molecular sciences · 2025
    Review
  11. Article
  12. Review
  13. Article
  14. Pharmaceuticals (Basel, Switzerland) · 2025
    Article
  15. Review
  16. Article
  17. Article
  18. Vitexin enhances radiosensitivity of mouse subcutaneous xenograft glioma by affecting the miR-17-5p/miR-130b-3p/PTEN/HIF-1α pathway.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2024
    Article
  19. 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

4 authors at 1 institution in 1 country.

Xiaoli LiuDepartment of Integrated Chinese and Western Medicine, Affiliated Cancer Hospital of Zhengzhou University & Henan Cancer Hospital, No. 127 Dongming Road, Zhengzhou City, 450008, Henan Province, People's Republic of China.
Qingfeng JiangDepartment of Integrated Chinese and Western Medicine, Affiliated Cancer Hospital of Zhengzhou University & Henan Cancer Hospital, No. 127 Dongming Road, Zhengzhou City, 450008, Henan Province, People's Republic of China.
Huaimin LiuDepartment of Integrated Chinese and Western Medicine, Affiliated Cancer Hospital of Zhengzhou University & Henan Cancer Hospital, No. 127 Dongming Road, Zhengzhou City, 450008, Henan Province, People's Republic of China.
Suxia LuoDepartment of Integrated Chinese and Western Medicine, Affiliated Cancer Hospital of Zhengzhou University & Henan Cancer Hospital, No. 127 Dongming Road, Zhengzhou City, 450008, Henan Province, People's Republic of China. luosxrm@163.com.
Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCurrently, the prognosis of patients with non-small cell lung cancer (NSCLC) remains dismal; hence, it is critical to identify effective anti-NSCLC agents with limited side effects. This study aimed to evaluate the therapeutic potential of flavonoid compound vitexin in human NSCLC cells and the underlying mechanisms.

resultsThe experimental results indicated that vitexin reduced the viability of A549 cells in a dose-dependent manner with nearly no toxicity against normal human bronchial epithelial 16HBE cells. Vitexin also dose-dependently increased A549 cell apoptosis, accompanied by the decreased Bcl-2/Bax ratio and the increased expression of cleaved caspase-3. Moreover, the in vivo anticancer activity of vitexin was further determined in nude mice bearing A549 cells. In addition, vitexin induced the release of cytochrome c from the mitochondria to the cytosol and the loss of mitochondrial membrane potential. Vitexin also significantly reduced the levels of p-PI3K, p-Akt and p-mTOR, and the pro-apoptotic effect of vitexin on A549 cells was partly blocked by SC79, an Akt activator.

conclusionsAccordingly, we believed that vitexin could be used as a potential therapeutic agent for the treatment of NSCLC in the future.

Indexed as

A549 CellsAnimalsAntineoplastic AgentsApigeninApoptosisCarcinoma, Non-Small-Cell LungCell Line, TumorCell ProliferationHumansLung NeoplasmsMembrane Potential, MitochondrialMiceMice, NudeMitochondriaPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAntineoplastic AgentsApigeninMTOR protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesvitexinMitochondrial dysfunctionNon-small cell lung cancerPI3K/Akt/mTOR signalingVitexin

Identifiers

PMID30797236
PMCPMC6387544
OpenAlexW2943723389

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Registered trials

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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.