Evidence map›Paper›PMID 31922221›Full record

ArticleMolecular medicine reports2020

Isoferulic acid inhibits human leukemia cell growth through induction of G2/M‑phase arrest and inhibition of Akt/mTOR signaling.

Zhiguo Long, Guangjia Feng, Na Zhao, Lei Wu, Hongbo Zhu

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

15 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Isoferulic acid suppressesFrontiers in microbiology · 2026
    Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Effect ofInternational journal of molecular sciences · 2023
    Article
  12. Article
  13. Article
  14. Article
  15. 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 2 institutions in 1 country.

Zhiguo Long *Department of Hematology, Shanghai Pudong Hospital, Fudan University, Shanghai 201399, P.R. China.
Guangjia Feng *Department of Hematology, Shanghai Pudong Hospital, Fudan University, Shanghai 201399, P.R. China.
Na ZhaoDepartment of Hematology, Shanghai Pudong Hospital, Fudan University, Shanghai 201399, P.R. China.
Lei WuDepartment of Hematology, Shanghai Pudong Hospital, Fudan University, Shanghai 201399, P.R. China.
Hongbo ZhuDepartment of Pathology, Shanghai Pudong Hospital, Fudan University, Shanghai 201399, P.R. China.
Fudan University · CNPudong Medical Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hematologic malignancy is a serious disease that develops quickly and aggressively, severely threatening human health owing to its high mortality. The current study aimed to evaluate the antitumor effects of isoferulic acid (IFA) on leukemia cells and investigate the possible molecular mechanisms. Hematologic cancer cell lines (Raji, K562 and Jurkat) were treated with IFA in a dose‑dependent manner and proliferation was measured by a cell proliferation assay. Cell cycle arrest was detected via flow cytometry using propidium iodide (PI) staining. Cell apoptosis and apoptosis‑associated signal pathways were analyzed via Annexin V/PI staining and western blot assays, respectively. IFA inhibited cell viability, induced cell apoptosis and triggered cell cycle arrest in G2/M phase in Raji, K562, and Jurkat cells in a dose‑dependent manner. In response to IFA treatment, the levels of cleaved poly(ADP‑ribose) polymerase and cleaved caspase‑3 were increased in Jurkat and K562 cells, which was associated with increased phosphorylation of Cdc2 and reduction of Cyclin B1 levels. IFA remarkably attenuated the phosphorylation of mTOR and Akt in Jurkat cells. Collectively, the present data suggested that IFA had therapeutic effects on Jurkat, K562, and Raji cells, indicating it as a promising candidate for the treatment of hematologic malignancy.

Indexed as

LeukemiaCinnamatesG2 Phase Cell Cycle CheckpointsHumansJurkat CellsK562 CellsM Phase Cell Cycle CheckpointsProto-Oncogene Proteins c-aktSignal TransductionTOR Serine-Threonine KinasesCinnamatesisoferulic acidProto-Oncogene Proteins c-aktTOR Serine-Threonine Kinasesakt/mTor signalingapoptosiscell cycle arresthematologic malignancyisoferulic acid

Identifiers

PMID31922221
PMCPMC7002969
OpenAlexW2999761189

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.