Evidence map›Paper›PMID 32944531›Full record

ArticleTranslational andrology and urology2020

Vitexin suppresses renal cell carcinoma by regulating mTOR pathways.

Yuhong Li, Qinghai Sun, Hui Li, Bin Yang, Meng Wang

Open access · diamondAbstract read
In one paragraph

Article in Translational andrology and urology, 2020. 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
1.2field-weighted citation impact, top 22% 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, 23 citations in OpenAlex.

  1. Article
  2. Review
  3. Molecular Mechanisms of Vitexin: An Update on Its Anti-Cancer Functions.International journal of molecular sciences · 2025
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Comparative Metabolomics study of flavonoids in the pericarp of different coloured bitter gourds (Physiology and molecular biology of plants : an international journal of functional plant biology · 2022
    Article
  10. Review
  11. Article
  12. The Hallmarks of Flavonoids in Cancer.Molecules (Basel, Switzerland) · 2021
    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.

Yuhong LiDepartment of Pharmacy, The First People's Hospital of Jingmen, Jingmen, China.
Qinghai SunClinical Medicine Discipline, Weifang Traditional Chinese Hospital, Weifang, China.
Hui LiDepartment of Medicine, Jining No. 1 People's Hospital, Jining, China.
Bin YangDepartment of Vascular Surgery, Jining No. 1 People's Hospital, Jining, China.
Meng WangDepartment of Medicine, Jining No. 1 People's Hospital, Jining, China.
Jining First People's Hospital · CNFirst People’s Hospital of Jingmen · CNWeifang Chinese Medicine Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRenal cell carcinoma (RCC) is one of the most common malignant tumors in the world. Vitexin (apigenin-8-C-D-glucopyranoside), a bioactive compound isolated from a variety of plants, has multiple protective effects on human health. The purpose of this study was to investigate the role of vitexin in RC and the related molecular mechanism.

methodsProliferation was tested with Cell Counting Kit-8 and Edu staining. Apoptosis was studied with flow cytometry. Immunofluorescent was applied to show LC3 spots. BALB/c nude mice bearing ACHN cells were established and immunohistochemical staining was applied to validate the in vivo effects of vitexin. All the effects and possible signaling pathways involved were validated with western blotting.

resultsSeventy micromole of vitexin started to show significant effect on the growth of normal renal tubular epithelial cells (HK-2), so 0, 10, 20 and 40 µM of vitexin were used in later experiments. Vitexin inhibited growth and induced apoptosis of ACHN and OS-RC-2 cells in a dose-dependent manner, and promoted excessive autophagy by reducing p62 levels and increasing Beclin1 and LC3II levels. Western blotting revealed that vitexin significantly increased the phosphorylation levels of Adenosine Monophosphate Activated Protein Kinase (AMPK) and c-Jun N-terminal kinase (JNK) in ACHN and OS-RC-2 cells, while decreasing the phosphorylation levels of phosphatidylinositol 3-kinase/activates protein kinase/mammalian target of rapamycin (PI3K/AKT/mTOR). In BALB/c nude mice bearing ACHN cells, vitexin inhibited tumor growth, reduced Ki67 and increased caspase-3 levels in the tumor tissues.

conclusionsThe results indicated that the tumor suppressive role of vitexin in ACHN and OS-RC-2 cells involved AMPK/mTOR, PI3K/AKT/mTOR, and JNK pathways. Therefore, vitexin may be a promising drug for the treatment of RCC.

Indexed as

AMPK/mTORautophagyc-Jun N-terminal kinase (JNK)phosphatidylinositol 3-kinase/activates protein kinase/mammalian target of rapamycin (PI3K/AKT/mTOR)Renal cell carcinoma (RCC)vitexin

Identifiers

PMID32944531
PMCPMC7475661
OpenAlexW3049449649

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.