Evidence map›Paper›PMID 41035965›Full record

ArticleOpen veterinary journal2025

Jauharotus Shobahah, Sri Puji Astuti Wahyuningsih, Dwi Winarni, Mochammad Aqilah Herdiansyah, M Ainun Najib Aly

Abstract read
In one paragraph

Article in Open veterinary journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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.

Jauharotus ShobahahDoctoral Program of Mathematics and Natural Sciences, Faculty of Science and Technology, Universitas Airlangga, Surabaya, Indonesia.
Sri Puji Astuti WahyuningsihDepartment of Biology, Faculty of Science and Technology, Universitas Airlangga, Surabaya, Indonesia.
Dwi WinarniDepartment of Biology, Faculty of Science and Technology, Universitas Airlangga, Surabaya, Indonesia.
Mochammad Aqilah HerdiansyahDepartment of Biology, Faculty of Science and Technology, Universitas Airlangga, Surabaya, Indonesia.
M Ainun Najib AlyFaculty of Pharmacy, Universitas Airlangga, Surabaya, Indonesia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: The potential anticancer properties of vitamin D3 (cholecalciferol) have garnered growing interest. Epidemiological and preclinical studies suggest an inverse correlation between vitamin D3 levels and CRC incidence. However, the precise molecular mechanisms and direct targets through which vitamin D3 exerts anticancer effects remain inadequately characterized. Aim: This study aimed to investigate the dual-targeting potential of vitamin D3 against two key oncogenic proteins involved in the pathogenesis of CRC: cyclin-dependent kinase 2 (CDK2), a critical regulator of cell cycle progression, and B-cell lymphoma 2 (Bcl-2), an anti-apoptotic protein implicated in tumor survival. Method: Molecular docking was performed to assess the binding affinity of vitamin D3 to CDK2 and Bcl-2. Molecular dynamics simulations were used to evaluate the stability of the docked complexes over time. Absorption, distribution, metabolism, excretion, and toxicity (ADMET) analysis was performed to predict the pharmacokinetics and safety profile of vitamin D3. Results: Docking analysis revealed strong binding affinities of vitamin D3 to both CDK2 (-9.5 kcal/mol) and Bcl-2 (-8.2 kcal/mol), suggesting stable interactions at the ATP-binding site of CDK2 and the BH3-binding groove of Bcl-2. Molecular dynamics simulations confirmed the conformational stability and sustained interactions of vitamin D3 with both targets throughout the simulation period. ADMET predictions indicated favorable oral bioavailability, low toxicity, and acceptable absorption and distribution characteristics, although solubility and plasma protein binding were limited. Conclusion: This study provides the first computational evidence that vitamin D3 may exert anticancer effects in CRC via dual mechanisms-cell cycle arrest through CDK2 inhibition and apoptosis induction through Bcl-2 modulation. These findings offer a novel perspective on the therapeutic repositioning of vitamin D3 as a multi-target agent in CRC management and warrant further validation through in vitro and in vivo studies.

Indexed as

Antineoplastic AgentsCholecalciferolColorectal NeoplasmsCyclin-Dependent Kinase 2Proto-Oncogene Proteins c-bcl-2AnimalsHumansMolecular Docking SimulationMolecular Dynamics SimulationAntineoplastic AgentsCDK2 protein, humanCholecalciferolCyclin-Dependent Kinase 2Proto-Oncogene Proteins c-bcl-2Bcl-2CDK2Colorectal cancerMolecular dockingvitamin D3

Identifiers

PMID41035965
PMCPMC12483463

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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.