Evidence map›Paper›PMID 32039440›Full record

ArticleBioscience reports2020

Isorhamnetin inhibited the proliferation and metastasis of androgen-independent prostate cancer cells by targeting the mitochondrion-dependent intrinsic apoptotic and PI3K/Akt/mTOR pathway.

Fangzhen Cai, Yanmei Zhang, Jianwei Li, Sihuai Huang, Ruilin Gao

Open access · goldAbstract read
In one paragraph

Article in Bioscience reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 2 pooled it
3.2field-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

32 citing papers in PubMed, 2 syntheses or guidelines pooled it, 58 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
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  11. Physiology and molecular biology of plants : an international journal of functional plant biology · 2024
    Review
  12. Review
  13. Article
  14. Isorhamnetin: what is theFrontiers in pharmacology · 2024
    Review
  15. Article
  16. Article
  17. Targeting PI3K/Akt signaling in prostate cancer therapy.Journal of cell communication and signaling · 2023
    Review
  18. Isorhamnetin exerts anti-tumor activity in DEN + CClMedical oncology (Northwood, London, England) · 2023
    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.

Fangzhen CaiDepartment of Urology, The Second Affiliated Hospital of Fu Jian Medical University, Quanzhou 362000, China.
Yanmei ZhangDepartment of Urology, The Second Affiliated Hospital of Fu Jian Medical University, Quanzhou 362000, China.
Jianwei LiDepartment of Urology, The Second Affiliated Hospital of Fu Jian Medical University, Quanzhou 362000, China.
Sihuai HuangDepartment of Urology, The Second Affiliated Hospital of Fu Jian Medical University, Quanzhou 362000, China.
Ruilin GaoDepartment of Urology, The Second Affiliated Hospital of Fu Jian Medical University, Quanzhou 362000, China.
Fujian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The present study investigated the effects of Isorhamnetin on two types of prostate cancer cells (androgen-independent and androgen-dependent) and explored its possible mechanisms underlying such effects. Treatment with Isorhamnetin significantly inhibited cell growth and induced lactate dehydrogenase (LDH) release of androgen-independent DU145 and PC3 prostate cancer cells, but exhibited almost no toxicity effect on androgen-dependent LNCaP prostate cancer cell line or normal human prostate epithelial PrEC cells, which was achieved by the induction of apoptosis in a mitochondrion-dependent intrinsic apoptotic pathway. Furthermore, Isorhamnetin inhibited cell migration and invasion in concentration-dependent manners by enhancing mesenchymal-epithelial transition (MET) and inhibiting matrix metalloproteinase (MMP) 2 (MMP-2) and MMP-9 overexpression. In addition, Isorhamnetin also down-regulated the expression of phosphorylated PI3K (p-P13K), Akt (p-Akt), and mTOR (p-mTOR) proteins in both cancer cells, revealing Isorhamnetin to be a selective PI3K-Akt-mTOR pathway inhibitor. In summary, these findings propose that Isorhamnetin might be a novel therapeutic candidate for the treatment of androgen-independent prostate cancer.

Indexed as

AndrogensApoptosisCell Line, TumorCell MovementCell ProliferationChinaHumansMaleMatrix Metalloproteinase 2Matrix Metalloproteinase 9MitochondriaNeoplasm MetastasisPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsPhosphorylationProstatic Neoplasms3-methylquercetinAndrogensMatrix Metalloproteinase 2Matrix Metalloproteinase 9MTOR protein, humanPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktQuercetinReceptors, AndrogenTOR Serine-Threonine KinasesApoptosisIsorhamnetinMetastasisPI3K/Akt/mTORProstate cancer

Identifiers

PMID32039440
PMCPMC7080645
OpenAlexW3005735644

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.