Evidence map›Paper›PMID 40296014›Full record

ArticleBMC cancer2025

Zapotin mitigates breast cancer progression by targeting PKCε mediated glycolytic pathway regulation.

Khushbukhat Khan, Maryam Anwar, Yasmin Badshah, Naeem Mahmood Ashraf, Arslan Hamid, Janeen H Trembley, Maria Shabbir, Tayyaba Afsar, Fohad Mabood Husain, Dilawar Khan and 1 more

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Article in BMC cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

11 authors.

Khushbukhat KhanDepartment of Biomedicine, Atta-ur-Rahman School of Applied Biosciences (ASAB), National University of Sciences and Technology (NUST), Islamabad, 44000, Pakistan.
Maryam AnwarDepartment of Biomedicine, Atta-ur-Rahman School of Applied Biosciences (ASAB), National University of Sciences and Technology (NUST), Islamabad, 44000, Pakistan.
Yasmin BadshahDepartment of Biomedicine, Atta-ur-Rahman School of Applied Biosciences (ASAB), National University of Sciences and Technology (NUST), Islamabad, 44000, Pakistan.
Naeem Mahmood AshrafSchool of Biochemistry & Biotechnology, University of the Punjab, Lahore, Pakistan. naeem.sbb@pu.edu.pk.
Arslan HamidLIMES Institute (AG-Netea), University of Bonn, Carl-Troll-Str. 31, 53115, Bonn, Germany.
Janeen H TrembleyDepartment of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, MN, USA.
Maria ShabbirDepartment of Biomedicine, Atta-ur-Rahman School of Applied Biosciences (ASAB), National University of Sciences and Technology (NUST), Islamabad, 44000, Pakistan.
Tayyaba AfsarDepartment of Community Health Sciences, College of Applied Medical Sciences, King Saud University, Riyadh, Saudi Arabia.
Fohad Mabood HusainDepartment of Food Science and Nutrition, College of Food and Agriculture Sciences, King Saud University, Riyadh, Saudi Arabia.
Dilawar KhanDepartment of Biomedicine, Atta-ur-Rahman School of Applied Biosciences (ASAB), National University of Sciences and Technology (NUST), Islamabad, 44000, Pakistan.
Suhail RazakDepartment of Community Health Sciences, College of Applied Medical Sciences, King Saud University, Riyadh, Saudi Arabia. smarazi@ksu.edu.sa.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe breast cancer recurrence and chemoresistance has increased over the years. A novel PKC, PKCε, may promote chemoresistance by causing hypoxia and cancer metabolic rewiring. A natural flavonoid, Zapotin, in colon cancer cells may modulate PKCε expression. Therefore, this study aimed to explore Zapotin impact on PKCε expression and the metabolic profile of breast cancer cells.

methodsPharmacophore analysis of Zapotin was performed and molecular dynamics (MD) simulations were employed to study PKCε and Zapotin interaction stability. The effect of Zapotin treatment on PKCε expression and various aspects of cancer cell viability and metabolism was studied in MCF-7 and MDA-MB-231 breast cancer cell lines using real-time PCR, growth and death assays, and Gas Chromatography-Mass Spectrometry.

resultsIn silico analyses revealed good solubility and absorption of Zapotin with lower toxicity. Zapotin showed cancer cell-specific cytotoxicity (P < 0.0001). It's treatment also reduced breast cancer cell viability, colony formation, and migratory potential by targeting PKCε and associated HIF-1ɑ and VEGF signaling (P < 0.01). Zapotin also impacted PKCε-mediated metabolic signaling by targeting glycolytic pathways.

conclusionThis study demonstrated the role of PKCε mediated HIF-1ɑ, VEGF, and glycolytic pathways in promoting breast carcinogenicity and demonstrated Zapotin as a potential treatment option for different types of breast tumors.

Indexed as

Breast NeoplasmsFlavonoidsGlycolysisProtein Kinase C-epsilonCell Line, TumorCell MovementCell ProliferationCell SurvivalDisease ProgressionFemaleGene Expression Regulation, NeoplasticHumansHypoxia-Inducible Factor 1, alpha SubunitMCF-7 CellsMolecular Dynamics SimulationSignal TransductionFlavonoidsHypoxia-Inducible Factor 1, alpha SubunitPRKCE protein, humanProtein Kinase C-epsilonBreast cancerMD simulationsMetabolic rewiringProtein kinase C epsilonZapotin

Identifiers

PMID40296014
PMCPMC12039207

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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Registered trials

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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.