Evidence map›Paper›PMID 40522383›Full record

ArticleMolecular biology reports2025

Vitamin D3 augments cytotoxic effect of Itraconazole on chronic myelogenous leukemia cell line: a synergic effect on AMPK/AKT signaling pathway.

Moein Tahvili, Vahid Nejati, Yaghub Pazhang

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

3 authors.

Moein TahviliDepartment of Biology, Faculty of Sciences, Urmia University, Urmia, Iran.
Vahid NejatiDepartment of Biology, Faculty of Sciences, Urmia University, Urmia, Iran. v.nejati@urmia.ac.ir.
Yaghub PazhangDepartment of Biology, Faculty of Sciences, Urmia University, Urmia, Iran. y.pazhang@urmia.ac.ir.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGrowing documents suggest combination therapy as an effective tool to treat the resistant cancer cells. Accordingly, in this study, it has been hypothesized that a combination of Vitamin D3(VD) and Itraconazole can inhibit Chronic Myeloid Leukemia(CML) K562 cells in vitro. METHODS AND

resultsK562 cells were incubated with different concentrations of either VD or Itraconazole either alone or in combination. The results showed that Itraconazole, VD, and combination treatment reduced the cell viability in a time and dose-dependent manner (P < 0.0001). In addition, the apoptosis rate was significantly induced in cells treated with combination drug (P < 0.0001). The Bax/Bcl-2 ratio was increased in treated cells, whereas the subcellular distribution of β-catenin protein was reduced. Morever, the phosphorylation of AKT and p65 were increased, whereas AMPK phosphorylation was decreased in treated cells (P < 0.0001).

conclusionOur results show that VD and Itraconazole synergically inhibit K562 cells viability via activation of AMPK and suppression of AKT function, suggesting that this combinational therapy potentially benefits CML patients.

Indexed as

AMP-Activated Protein KinasesCholecalciferolItraconazoleLeukemia, Myelogenous, Chronic, BCR-ABL PositiveApoptosisbeta CateninCell ProliferationCell SurvivalDrug SynergismHumansK562 CellsPhosphorylationProto-Oncogene Proteins c-aktSignal TransductionAMP-Activated Protein Kinasesbeta CateninCholecalciferolItraconazoleProto-Oncogene Proteins c-aktApoptosisCombination therapyItraconazoleK562 cell lineMyeloid leukemiaVitamin D3

Identifiers

What Socratic holds

Textmetadata
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 Socratic graph.